JID, Vol 145, Issue 11, Supp 1

ISSN: 0022-202X Vol 145, Issue 11, Supplement 1, 2025 Supplement to the Journal of Investigative Dermatology www.jidonline.org

6th Inflammatory Skin Disease Summit: The Translational Revolution November 12-15, 2025 The New York Academy of Medicine, New York City, NY, USA Meeting Organizers Emma Guttman-Yassky, MD, PhD Icahn School of Medicine at Mount Sinai, New York, NY, USA Patrick M. Brunner, MD, MSc Icahn School of Medicine at Mount Sinai, New York, NY, USA James G. Krueger, MD, PhD The Rockefeller University, New York, NY, USA Georg Stingl, MD Medical University of Vienna, Vienna, Austria Disclaimer: The 6th Inflammatory Skin Disease Summit: The Translational Revolution abstracts in this supplement have not been reviewed by Journal of Investigative Dermatology (JID) Editors. The abstracts were reviewed, selected, and approved for publication by the organizers of the 6th Inflammatory Skin Disease Summit The Translational Revolution. Neither Journal of Investigative Dermatology (JID), nor Elsevier are responsible for errors or omissions in the abstracts. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. Because of rapid advances in the medical sciences, in particular, independent verification of diagnoses and drug dosages should be made. To the fullest extent of the law, no responsibility is assumed by the publisher for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Although all advertising material is expected to conform to ethical and medical standards, inclusion in this publication does not constitute a guarantee or endorsement of the quality or value of such product or of the claims made of it by its manufacturer. Notice: Abstracts 29, 115, 119, 128, 171, 172, 173, 174, 175, 176, 177, 178, 179, 199, 216, 291, 312 and 365 have been withdrawn by the authors and therefore do not appear in this supplement. www.jidonline.org e31

1 Diagnosis of Castleman Disease in a Patient with Erythrodermic Psoriasis Ko Eun Kim1, Han-Na Kim1, Jiehyun Jeon1, Dae Sik Kim2 and Yoo Sang Baek1 1 Department of Dermatology, Korea University College of Medicine, Seoul, South Korea and 2 Division of Hematology-Oncology, Department of Internal Medicine, Korea University College of Medicine, Seoul, South Korea Castleman disease (CD) refers to a spectrum of polyclonal lymphoproliferative disorders that exhibit similar clinicopathological characteristics. It is categorized into two main types: unicentric CD (UCD), which generally presents without symptoms and follows a benign course, and multicentric CD (MCD), which typically involves systemic manifestations and may worsen over time. MCD includes idiopathic MCD (iMCD) and other subtypes based on the underlying cause. Several cases have been reported where CD coexists with psoriasis. This report discusses a 74-year-old woman with a long history of psoriasis who was later diagnosed with CD. Following a year without treatment, she developed an extensive erythematous, scaly rash along with recent fatigue and weight loss. Clinical assessment suggested erythroderma or exfoliative dermatitis, leading to the reinstatement of therapy with acitretin and topical corticosteroids. Laboratory findings showed notable anemia, an increase in peripheral myelocytes, and low albumin levels. She was referred to the hematology department and ultimately diagnosed with iMCD upon admission. This case underscores the rare coexistence of erythrodermic psoriasis and iMCD. 2 Dental Comorbidities in Patients with Psoriatic Arthritis: A Nationwide Population-Based Cohort Study Seokjin Kong1, Eun Jung Kwak2, Han-Na Kim3, Ko Eun Kim3, Jiehyun Jeon3, Chan Mi Park4 and Yoo Sang Baek3 1 Department of Biomedical Informatics, Korea University College of Medicine, Seoul, South Korea, 2 National Dental Care Center for Person with Special Needs, Seoul National University Dental, Hospital, Seoul, South Korea, 3 Department of Dermatology, Korea University College of Medicine, Seoul, South Korea and 4 Biomedical Research Center, Korea University Guro Hospital, South Korea Recent evidence suggests a link between psoriasis and dental comorbiditiess, particularly chronic periodontitis. Given the association between psoriasis and psoriatic arthritis, we investigated the prevalence of dental comorbidities in patients with psoriatic arthritis. Using nationwide claims data, we analyzed a cohort of patients with psoriatic arthritis (n =40,921) and age- and sex-matched controls (n =204,605). The incidence of dental caries, pulp and periapical disease, periodontal disease, gingival changes, and tooth loss was assessed. Adjusted hazard ratios showed significantly increased risks for dental caries (HR 1.264; 95% CI: 1.088—1.469), pulp and periapical disease (HR 1.705; 95% CI: 1.516—1.917), and periodontal disease (HR 1.205; 95% CI: 1.152—1.261) in the psoriatic arthritis group (p < 0.001). No significant associations were found for gingival changes or tooth loss. These findings suggest an elevated risk of dental comorbidities in patients with psoriatic arthritis. 3 (Neutrophil Extracellular Traps) NET-worth of Neutrophils in Psoriasis Debdeep Mitra Command Hospital Chandimandir, Panchkula, India Introduction: Recent advances have enhanced our understanding of the pathogenesis of psoriasis, a chronic inflammatory skin disease. Neutrophils, the most abundant white blood cells in circulation, are frequently observed in psoriatic lesions. These cells can release neutrophil extracellular traps (NETs)—web-like structures composed of decondensed chromatin, histones, and antimicrobial proteins—designed to trap and neutralize pathogens. While NETs are beneficial in host defense, emerging evidence implicates them in the development of autoimmune disorders such as systemic lupus erythematosus and rheumatoid arthritis. In psoriasis, neutrophil infiltration of the dermis and subsequent migration into the epidermis leads to the formation of Munro’s microabscesses and spongiform pustules. Clinical observations suggest a pathogenic role for neutrophils, as disease remission has been noted with neutropenia, and flares are associated with restoration of neutrophil counts. Moreover, neutrophils have been shown to express interleukin-17 (IL-17) in psoriatic skin, further supporting their contribution to disease mechanisms. Methods: This study assessed NET levels in the peripheral blood of patients with plaque psoriasis (n =30) compared to age- and gender- matched healthy individuals (n =30). We evaluated correlations between NET levels, disease severity, and response to treatment. Results: Patients with psoriasis demonstrated a significantly higher number of NET-forming neutrophils in peripheral blood compared to healthy controls. A positive correlation was found between the quantity of NETs and the severity of skin involvement. However, NET levels did not show a significant association with the severity of psoriatic arthritis. NET levels also showed a positive correlation with pustular psoriasis (p<0.05) &can be a marker to assess response to treatment. Conclusions: Elevated NET formation is associated with increased disease activity in plaque psoriasis. These findings suggest that NETs may serve as a potential biomarker for disease monitoring. Additionally, targeting NET formation could offer a novel therapeutic strategy to modulate inflammation and manage psoriasis progression. 4 Case Control trial to evaluate the Cytokine response to the use of Capsule Thalidomide in Erythema nodosum leprosum Debdeep Mitra Command Hospital Chandimandir, Panchkula, India Leprosy, caused by Mycobacterium leprae,can be complicated by Type-II-lepra reaction—Erythema Nodosum Leprosum(ENL)—an acute inflammatory episode resembling sepsis, with fever, widespread inflammation, and neutrophil elevation. Early identification and prompt management are vital to prevent nerve injury and permanent disability. Although thalidomide is highly effective in controlling ENL through its immunomodulatory action, its use is limited in women of childbearing age because of teratogenic risks. In this investigation, we evaluated three immunological indicators—Interferon-γ, Tumor Necrosis Factor-α(TNF-α), &CD64 expression on circulating neutrophils—to determine their association with ENL severity and their responsiveness to thalidomide therapy. We carried out a case-control study at a tertiary care hospital in New Delhi. Leprosy patients were diagnosed clinically and by slit-skin smear, then classified by the Ridley—Jopling system. Those experiencing ENL comprised the case group, while healthy individuals matched for age, sex,&geographic origin served as controls. Blood samples were drawn from all participants at enrollment, and a second sample was obtained from ENL patients seven days after starting thalidomide. We performed histopathological examination, immunofluorescence staining, immunohistochemistry, RT-PCR assays, and flow cytometry to quantify cytokine levels and measure CD64on neutrophils. Our results demonstrated that CD64expression on neutrophils was markedly higher in ENL patients than in controls and increased proportionally with clinical severity. Both Interferon-γand TNF-αconcentrations were significantly elevated in ENL cases, underscoring their value as diagnostic markers. After one week of thalidomide therapy, CD64 levels declined in parallel with clinical improvement, whereas cytokine levels showed no consistent post-treatment change. These findings indicate that neutrophil CD64 is a reliable biomarker for ENL activity and a practical tool for monitoring thalidomide effectiveness. Furthermore, CD64 may represent a novel therapeutic target, especially for patients who cannot receive thalidomide. Future studies should explore CD64 inhibition and broader applications of thalidomide’s immunomodulatory effects in other diseases driven by neutrophilic inflammation, such as sepsis. 5 Prospective case-control study to examine inflammatory indicators and markers to predict Staphylococcal scalded skin syndrome Debdeep Mitra Command Hospital Chandimandir, Panchkula, India Introduction: Staphylococcal Scalded Skin Syndrome (SSSS) is an acute dermatological condition predominantly affecting infants and young children, with rare adult presentations. Early diagnosis is crucial but often challenging due to the lack of rapid diagnostic tools or standardized clinical scoring systems. Differentiating SSSS from other skin eruptions such as maculopapular rashes at initial presentation remains a clinical hurdle. This study aims to identify reliable clinical and serological markers for early diagnosis and assess their association with disease severity and systemic involvement. Methods: A prospective observational study was conducted involving 25 patients diagnosed with SSSS and 25 control patients presenting with maculopapular eruptions. Various clinical parameters and serum biomarkers were analyzed, including thymus and activation-regulated chemokine (TARC), high-sensitivity C-reactive protein (hsCRP), white blood cell counts, liver enzymes, and neutrophil extracellular traps (NETs). Statistical models were used to evaluate their diagnostic accuracy and predictive value for disease severity. Results: Serum TARC levels above 612.25 pg/mL, total body surface area (TBSA) involvement over 30%, hsCRP >5 mg/L, leukocytosis >12×109/L, and elevated AST (>90 U/L) were found to significantly distinguish SSSS from maculopapular rashes. While TARC served as a sensitive screening biomarker, it did not predict disease severity or outcome. Conversely, NET levels correlated strongly with the severity of SSSS and length of hospitalization. A composite diagnostic model using TBSA, neutrophil percentage, and hsCRP outperformed individual markers. The derived equation— Odds of SSSS =Antilog [-11.26 + 0.3(TBSA) + 0.3(hsCRP) —0.1(neutrophil %)]—achieved 96% sensitivity and 100% specificity at a cutoff value of 7.8. Conclusions: This study presents a practical and accurate diagnostic tool for SSSS suitable for resource-limited settings. Early application of this model can guide timely therapy and reduce unnecessary investigations. Additionally,NET levels show promise as prognostic indicators in severe cases of SSSS. Neutrophil extracellular traps showed positive correlation to response to treatment. 6 A Randomized, Double-Blind, Placebo-Controlled Trial Evaluating the Effectiveness of Omalizumab, an Anti-IgE Monoclonal Antibody, in Alleviating Itch Associated with Chronic Spontaneous Urticaria in pediatric population Debdeep Mitra Command Hospital Chandimandir, Panchkula, India Introduction: Chronic spontaneous urticaria (CSU) in children manifests as recurring itchy wheals—with or without deeper swelling—that persist for at least six weeks. Although it affects just under 1% of school-aged youngsters, its toll on daily life and well-being is considerable. Standard therapy relies on H1-antihistamines, yet many 6-to-12-year-olds continue to suffer relentless outbreaks. While systemic steroids or immunosuppressive agents can bring relief, their use in this age group raises serious safety concerns. Omalizumab, a targeted anti-IgE antibody approved for asthma and atopic dermatitis, may offer a safer option, but its place in treating pediatric CSU remains poorly defined. This trial sought to determine whether omalizumab could safely and effectively control moderate-to-severe CSU in antihistamine-resistant children. Methods: We conducted a double-blind, placebo-controlled study involving 30 children aged 6—12years who experienced moderate-to-severe CSU despite optimized antihistamine treatment. Participants were randomized in equal numbers to receive either 150mg of omalizumab or placebo via subcutaneous injection every four weeks for four doses. After completing the dosing phase, children were observed for an additional 16 weeks. At baseline, both groups were similar in age distribution, gender, and serum IgE concentrations. Disease severity was tracked using the Urticaria Activity Score(UAS), which averaged 5.7(range 4—6) at study entry. Results: By week 16, children receiving omalizumab demonstrated a pronounced decrease in serum IgE levels and lower expression of the high-affinity IgE receptor (FcεRI) on circulating basophils and plasmacytoid dendritic cells (p<.001 versus placebo). Corresponding clinical improvement was reflected in UAS, which fell sharply in the omalizumab group at both 16&32 weeks,whereas scores in the placebo group showed minimal change. Conclusions: In antihistamine-refractory pediatric CSU, omalizumab produced significant reductions in immunologic markers and symptom scores, with an excellent safety profile. These findings support omalizumab as a viable treatment for children whose urticaria persists despite standard therapy, offering both symptomatic relief &improved life quality. e32 Journal of Investigative Dermatology (2025), Volume 145 ABSTRACTS | Abstracts from the 6th Inflammatory Skin Disease Summit

7 Perceptions of Pain Management Among Patients with Hidradenitis Suppurativa (HS), with Special Emphasis on the Experiences of Those Who Have Been Pregnant Alicia Edwards1, Savanna Vidal2, Nikita Menta2 and Adam Friedman2 1 Howard Univeristy College Of Medicine, Washington, United States of America and 2 George Washington School of Medicine, Washington, United States of America Hidradenitis Suppurativa (HS) is a chronic, inflammatory skin disease marked by painful lesions that significantly impact patients’ quality of life (Goldburg, 2020). Pain remains one of the most debilitating aspects of HS, yet patient experiences related to pain management especially during pregnancy are poorly understood (Surapaneni, 2024, Perng, 2016) This study aimed to assess perceptions of pain and management among individuals with HS, with an emphasis on those who have experienced pregnancy. The goal was to explore differences in pain perception, management strategies, and provider communication between those with and without pregnancy history, while also examining how race, ethnicity, and demographic factors influence treatment experiences. A validated online survey was disseminated via HS Connect and completed by 202 individuals with HS. The survey captured demographic data, HS clinical history, pain levels during various activities, symptom severity, pain management strategies, and comfort discussing pain and pain management with healthcare providers. Respondents were stratified into two tiers: those with a history pregnancy (Tier 1) and those without (Tier 2). Statistical analyses, including Kruskal—Wallis and Chi-squared tests, were used to assess associations between ethnicity and pregnancy-related outcomes and behaviors. Of the respondents, 92 (45.54%) had experienced pregnancy and 110 (54.46%) had not. Pain scores were higher during non-pregnant states, and both groups cited stigma, dismissal, and discomfort discussing pain with providers. Only 4.44% of respondents received pregnancy-specific pain guidance. No significant associations were found between ethnicity and birth outcomes, pain levels, medication use, or provider support. Qualitative responses highlighted systemic gaps, provider mistrust, and cultural stigmas around pain treatment. Patients with HS, particularly those navigating pregnancy, face major gaps in pain management support (Perng, 2016). Findings underscore the urgent need for improved provider education, culturally competent care, and development of safe, effective pain management protocols for pregnant individuals with HS. 8 The Role of IL-15Ra Trans- and Cis-Presentation in Vitiligo Pathogenesis Fateme Rajabi, Ken Okamura, Xueli Fan, Nuria Martinez, Chinmayee Dash and John Harris Department of Dermatology, University of Massachusetts Chan Medical School, Worcester, United States of America Vitiligo, a depigmenting skin condition affecting ∼1% of the population, is caused by destruction of melanocytes by CD8+ T cells. After the initial immune response, a fraction of these skin-infiltrating CD8+ T cells, referred to as resident memory T cells (Trm), undergo reprogramming, enabling them to persist within the skin and contribute to disease maintenance and recurrence. IL-15 plays a critical role in the formation and function of Trm cells. In the skin, IL-15 is produced by keratinocytes and dendritic cells (DC). These cells trans-present IL-15 through the monomeric IL-15α receptor to the heterodimeric IL-15Rβ/γ receptor expressed on Trms. IL-15Rαis also expressed on Trm cells, where it forms a trimeric receptor with IL-15Rβ/γand through cis-presentation of IL-15, amplifies the response to the cytokine. Our previous work in our vitiligo mouse model revealed that blocking IL-15Rβ reduced Trm counts and enhanced durable repigmentation. To assess the role of cis-presentation by the trimeric receptor, we used CD8+ T cells from IL-15Rα knockout (KO) TCR transgenic mice (PMEL) to induce vitiligo. No significant changes in vitiligo severity, T cell infiltration, or effector function were observed. We explored the role of trans-presentation by knocking out IL-15Rαin recipient mice. We saw lower PMEL/Trm infiltrating the skin without much change in the vitiligo scores at week 7 compared to controls. However, repigmentation was faster and more pronounced. To determine the most critical cell type, we performed an experiment using IL15RαDCs to induce vitiligo, which showed comparable results to controls. Next, we focused on keratinocytes, using a keratinocyte-specific KO. We saw reduced severity of depigmentation (p=0.04) at week 7 and decreased Trms in skin (p<0.0001). These findings emphasize the key role of IL-15Rα trans-presentation by keratinocytes for vitiligo induction and persistence in vivo, whereas cis-presentation plays a less critical role. 10 Therapeutic Efficacy of 2% Mupirocin in Managing Staphylococcus aureus and Streptococcus pyogenes Wound Infections Paola Rivera1, Marc Bello, Geraldo Brito, Gabriela Pichardo, Elias Cruz and Daisy Blanco 1 Instituto Dermatolo´gico Dominicano y Cirugı´a de Piel Dr. Huberto Bogaert, Dominican Republic Background: Skin and soft tissue infections range from mild to severe and are increasingly complicated by antibiotic resistance, particularly involving Staphylococcus aureus and Streptococcus pyogenes. Mupirocin, a topical antibiotic, is effective against these pathogens. This quasi-experimental study evaluated the short-term efficacy and safety of 2% topical mupirocin cream in treating superficial traumatic and surgical wounds infected with S. aureus and/or S. pyogenes in mostly pediatric patients at the Dominican Dermatological Institute and Skin Surgery “Dr. Huberto Bogaert D´ıaz.” Methodology: Between January and April 2023, patients with clinically infected wounds were treated with 2% mupirocin cream applied three times daily for 10 days. Efficacy was measured using the Severity of Infected Wounds Scale (SIRS), which scores erythema, swelling, discharge, and local warmth (0—3 each; max score 12). A therapeutic response was defined as a ≥50% reduction in the SIRS score by day 11. Adverse effects were monitored via physical exam and patient interviews. Results: Of 135 patients, 134 (99.2%) showed a favorable response without adverse effects. Only one patient (0.7%) developed a rash requiring treatment discontinuation. Pathogens isolated included S. aureus (56.3%), S. pyogenes (2.2%), and both (41.5%). Conclusions: Topical 2% mupirocin cream proved highly effective and well tolerated for superficial wounds infected with S. aureus and/or S. pyogenes. Its excellent safety profile and efficacy support its role as a first- line treatment, potentially reducing the need for systemic antibiotics and contributing to antimicrobial stewardship. 11 Discovery of Spaceflight-Induced Cell Cycle Dysregulation with Igf2-Mediated Cell Cycle Restabilization in Mice Yash Bhuva, Azimullah Rifai, Pakhi Gupta and Shreya SrikanthNASA Ames Research Center, Sunnyvale, United States of America From the moment when humans made their first venture into space, it has been noticed that spaceflight has many impacts on the human body, particularly related to skin health and wound healing. To identify roots to this problem, we investigated the OSD-254 “Transcriptional analysis of dorsal skin from mice flown on the RR-7 mission” dataset where we identified down-regulation of genes involved in cell cycle regulation (Cdk1, Ccnb1, Ccnb2) in female C57BL/6J mus musculus. This trend is also reflected in homo sapiens, where according to literature, microgravity induces dysregulation in cell cycle genes in human cells (Verma et al., 2015). Additionally, cell cycle genes have been established to be keystone in cellular proliferation, where Cdk1, Ccnb1, and Ccnb2 have been found to be upregulated in various cancers. These genes are connected to cellular proliferation and development, specifically in their roles of regulating the G2/M transition phase of the cell cycle. In our investigation, we also found Igf2, which was upregulated in space, to be involved in many cell growth and proliferative processes along with these three regulatory genes. Through further analysis, we found their direct cellular interactions within the MAPK pathway. We then identified Igf2’s role in enhancing skin health (skin thickness/differentiated cell concentration) and wound healing (Ward et al., 2003) as well its role in metabolic pathways. This led us to focus on identifying unique metabolic profiles characterized by Igf2 expression in microgravity conditions. By designing an experiment utilizing immunofluorescence (IF), AO/PI flow cytometry assays, histological assessments, metabolomic assays, and other procedures to examine impacts of cell cycle gene dysregulation and Igf2 expression on mice skin health/metabolomic characteristics, we aim to understand underlying mechanisms. This knowledge will open doors to tailor solutions for microgravity impacts on skin health whilst identifying potential metabolic side effects. 12 Inhibition of the JAK/STAT pathway prevents acantholysis in pemphigus Farzan Solimani, Julia Holstein, Katharina Meier, Alberto Mesas-Fernandez, Yun-Fei Jiang, Maria Feoktistova, Morna Friederike Schmidt, Amir Yazdu, Franz Joachim Hilke and Kamran Ghorerschi Charite´ - Universita¨tsmedizin Berlin, Berlin, Germany Pemphigus is a severe autoimmune blistering disorder of skin and mucosa which is elicited by gG autoantibodies targeting desmosomal components such as desmoglein 3 (Dsg3). Keratinocytes lose cytoarchitectural stability and reciprocal adhesion in a process called acantholysis, which manifests as blisters and erosions. It is widely accepted that keratinocytes themselves can produce inflammatory factors such as cytokines in response to mechanical stress. This suggests that stress as induced by the binding of autoantibodies to Dsg3 might initiate similar effects in keratinocytes. In this work, we evaluate the cytokine response of human epidermal keratinocytes after treatment with anti-Dsg antibodies (AK23 and human pemphigus IgG). Quantitative gene expression (qPCR) was performed to study cytokine expression induced after AK23 treatment. Activation of the signal transducer and activation of transcription (STAT) factors and the impact of Janus kinase (JAK) inhibitors in anti-Dsg antibodies-treated keratinocytes were evaluated by western blotting and gene expression assays. Moreover, we studied the functional role of JAK inhibitors during anti-Dsg antibodies -induced cell dissociation by dispase assay. Epidermal activation of pSTATs in pemphigus and control skin was determined by immunohistochemistry. Finally, a pemphigus lesion in a steroid-unresponsive patient was treated with topical ruxolitinib, the clinical response and epidermal STAT activation were assessed. Our investigation revealed that loss of epidermal integrity by AK23 is accompanied by increased expression of cytokines (IL6, IL19, IL24, IFNE) and anti-Dsg antibodies activate STAT1 and STAT3. Administration of JAK inhibitors in vitro and in vivo prevented anti-Dsg antibodies-induced STAT activation and cell dissociation in keratinocytes. 13 OX40 expression limits suppressive capacity of FOXP3+ T regulatory cells in pemphigus Alberto Mesas-Ferna´ndez1, Kot Kokubo2, Alina Deland1, Edis Klein1, Katharina Meier1, Julia Holstein3, Christine Zimmer4, Franz J Hilke1, Christian Mo¨bs4, Michael Hertl4, Kiyoshi Hirahara2, Farzan Solimani1 and Kamran Ghoreschi1 1 Department of Dermatology, Charite´ - Universita¨tsmedizin Berlin, Berlin, Germany, 2 Department of Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan, 3 Department of Dermatology, Eberhard Karls Universita¨t Tu¨bingen, Tu¨bingen, Germany and 4 Department of Dermatology and Allergology, Philipps-Universita¨t Marburg, Marburg, Germany Pemphigus is a severe autoimmune disorder characterized by a breakdown in immunological tolerance, driven by autoreactive T and B cells against desmogleins (Dsg) 1 and 3, resulting in development of skin and mucosal blistering. T regulatory (Treg) cells, crucial for maintaining immune tolerance, are often impaired in autoimmune conditions. In this study, we characterized Treg cell subsets in pemphigus and identified a FOXP3+ Treg population that exhibits phenotypic and functional features associated with autoreactive T cells. This subset showed only minimal IL-10 expression and a reduced capacity to suppress effector T cell proliferation. Notably, these FOXP3+ Treg cells expressed high levels of OX40, co-stimulatory molecule and immune checkpoint protein. Blocking OX40 signaling restored their suppressive function and IL-10 production. Furthermore, by studying patients with pemphigus receiving B cell depleting therapies, we observed an increase of this non-suppressive FOXP3+ Treg population during clinical relapses. RNA sequencing of these Treg cells revealed a distinct transcriptional profile, including the upregulation of chemokine involved lymphocyte recruitment, chemotaxis and inflammatory responses. Additionally, this Treg subset exhibited enhanced capacity for skin migration, as indicated by increased expression of the cutaneous lymphoid antigen (CLA). Antigen-specific analysis revealed that the subset displayed a high reactivity to the pemphigus antigen, Dsg 3. Moreover, we detected a significant enrichment of OX40+ Treg cells in lesional skin of pemphigus patients, suggesting their contribution to disease pathology. Our findings highlight the functional heterogeneity of Treg cells in pemphigus and the role of the non-suppressive OX40+ FOXP3+ Treg subset. These results provide potential for new therapeutic targets in order to restore immune tolerance in pemphigus. Abstracts from the 6th Inflammatory Skin Disease Summit | ABSTRACTS www.jidonline.org e33

14 Common Psoriasis Therapeutics and Ocular Symptoms: Analysis of the FAERS Database Robert Adler, Tristi Edwards, Katerina Svigos and Jeannette Jakus SUNY Downstate Health Sciences University, Brooklyn, United States of America Psoriasis has been recognized as a disease with various extracutaneous manifestations, including ophthalmic symptoms. With a rise in the number of available anti-psoriatic medications, we sought to identify ocular adverse events (OAE) associated with psoriasis therapy. OAE for adalimumab, apremilast, etanercept, infliximab, ustekinumab, guselkumab, and secukinumab were queried from the FAERS Database with disproportionality analysis (DA) conducted for top 25 OAEs. Infliximab (15/25 conditions ROR>1) was associated with blepharospasm (ROR 159.60), uveitis (8.27), iritis (4.77), visual impairment (4.59) and retinal detachment (3.62). Adalimumab (18/25) was associated with blepharospasm (16.09), retinal tear (4.72), macular degeneration (5.15), retinal detachment (3.36), and cataracts (2.59). Etanercept (14/25) was associated with blepharospasm (15.77), iritis (2.30), increased lacrimation (1.636), cataracts (1.406), and uveitis (1.35). Secukinumab (16/25) was associated with blepharospasm (21.43), blepharitis (2.60), eye discharge (2.41), uveitis (2.16), and eyelid swelling (2.096). Ustekinumab (9/25) was associated with blepharospasm (35.66), uveitis (2.347), blepharitis (2.01), visual impairment (1.77), and cataracts (1.481). Guselkumab (4/ 25) was associated with macular degeneration (4.84), ulcerative keratitis (2.99), blepharitis (2.25), and glaucoma (1.04). Apremilast, however, was only associated with increased risk of blepharospasm (16.43); all other adverse events studied displayed no increased risk. Our findings support the necessity of physician guidance and the research needed in elucidating ocular adverse events. 15 Comorbidities Associated with Psoriasis Diagnosis: Analysis of the MEPS Questionnaire Robert Adler, Tristi Edwards, Katerina Svigos and Jeannette Jakus SUNY Downstate Health Sciences University, Brooklyn, United States of America Psoriasis is recognized as a systemic disease with various comorbidities that increase disease burden and complicate treatment. These systemic manifestations have a profound impact on patient quality of life. Data from the Medicare Expenditure Panel Survey (MEPS) between 2016 and 2022 was utilized to focus on 50 ICD-10 codes. Odds ratios (OR) with confidence intervals (CI) were used as measures of association between 926 psoriasis patients with 144,493 controls. The analysis revealed several significant associations across multiple systems (Table 1). The odds of developing hypertension (1.35, CI 1.2-1.52), dyslipidemia (1.45, CI 1.27-1.65), and arrhythmias (3.49, CI 2.52-4.82) were increased, although notably there was no increased risk of myocardial infarction (MI) (1.12, CI 0.75-1.68) or chronic ischemic heart disease (1.32, CI 0.99-1.76). Participants also had a higher rate of diabetes (1.38, CI 1.17-1.63), hypothyroidism (2.3 CI 1.84-2.88), gout (2.03, CI 1.42-2.89), and acid-base disorders (1.85, CI 1.25-2.73). Psoriasis patients were also more likely to have anxiety (1.55, CI 1.32-1.83), depression (1.59, CI 1.34-1.89), sleep disorders (1.87, CI 1.52-2.22), and migraine (1.50, CI 1.08-2.08). Our analysis highlights the diverse range of comorbid conditions associated with psoriasis, highlighting the need for comprehensive, multidisciplinary care. 16 Paradoxical Head and Neck Erythema Associated with Dupilumab in Severe Atopic Dermatitis: A Two-Year Retrospective Study Based on Serial Clinical Photographs Nam Gyoung Ha and Yong Hyun Jang Kyungpook National University Hospital, Daegu, South Korea Dupilumab has markedly improved disease control in patients with moderate-to-severe atopic dermatitis (AD), yet new-onset head and neck (H&N) erythema has emerged as a distinctive paradoxical reaction. This study aimed to characterize the incidence, clinical features, and risk factors associated with this phenomenon. A retrospective review was conducted in 50 patients with severe AD receiving dupilumab, all of whom underwent serial facial photography at baseline and at weeks 16, 40, 64, and 88. Erythema severity was graded using the Investigator Global Assessment (IGA) scale by two independent dermatologists. Among the cohort, 26 patients (52.0%) developed new-onset H&N erythema, which predominantly affected the medial cheeks (84.6%) and forehead (76.9%) in a bilateral (88.5%) and diffuse (84.6%) pattern. Oily skin was significantly associated with erythema development (odds ratio 6.53, p=0.008), and patients with pre-existing H&N dermatitis exhibited more severe erythema during treatment. These findings highlight the characteristic presentation and risk factors of this paradoxical reaction and suggest the need for proactive monitoring in susceptible individuals during dupilumab therapy. 17 Prevalence of Cardiovascular Disease in Prurigo Nodularis: A Systematic Review and Meta-Analysis Natalia Chalupczak1, Carmen Li1, Christy Chang2, Meredith Polaskey1 and Raj Chovatiya3 1 Chicago Medical School, Chicago, United States of America, 2 University of Illinois Chicago, College of Medicine, Chicago, United States of America and 3 3. Center for Medical Dermatology + Immunology Research, Chicago, United States of America Background: Prurigo nodularis (PN) is a chronic neuroinflammatory skin disorder characterized by persistent pruritus and nodular lesions. Emerging evidence suggests an association between PN and cardiovascular disease, but the precise prevalence remains unclear. Objective: To assess the prevalence of cardiovascular comorbidities in patients with PN through a systematic review and meta-analysis. Methods: A systematic search of Embase, PubMed, Scopus, and Cochrane Library was conducted following PRISMA guidelines (PROSPERO CRD42024574854). Meta-analysis using a random-effects model estimated pooled cardiovascular disease prevalence in patients with PN. Results: Nine studies including 20,381 patients with PN met the inclusion criteria. The pooled prevalence of hypertension was 31.2% [95% CI: 14.0%-48.3%] (n = 5,616), and congestive heart failure was 8.8% [1.5%-16.1%] (n =674), both with high heterogeneity (I2 >99%). Coronary artery disease prevalence was inconsistent across studies. Limitations: The small number of available studies, lack of matched control populations, and reliance on retrospective and cross- sectional data limit the ability to establish causality. Conclusion: Patients with PN have a high burden of cardiovascular diseases, particularly hypertension and heart failure. These findings highlight the need for cardiovascular screening in patients with PN and further research to clarify disease-specific risks and mechanisms. 18 Investigating the Relationship Between Chronic Inflammatory Skin Disease and Squamous Cell Carcinoma Natalia Chalupczak1, Amritpal Kooner2, Sophia Manduca3, Ramneek Dhami4, Rawle Sekhon5 and Bhavik Patel6 1 Chicago Medical School, Chicago, USA, 2 Chicago College of Osteopathic Medicine, Midwestern University, Downers Grove, USA, 3 New York University Grossman School of Medicine, New York, USA, 4 University of Nevada,Reno School of Medicine, Reno, USA, 5 Windsor University School of Medicine, St. Kitts, Caribbean and 6 Lincoln Memorial University DeBusk College of Osteopathic Medicine, Harrogate, USA Chronic inflammatory skin diseases may elevate the risk of squamous cell carcinoma (SCC) through prolonged immune dysregulation, chronic tissue damage, and cytokine-mediated pro-oncogenic signaling. This study aimed to evaluate associations between SCC and various chronic inflammatory dermatoses using the NIH All of Us database, which emphasizes inclusion of diverse and underrepresented populations. Individuals with SCC were identified using SNOMED and ICD-10 codes and matched 1:4 with controls via nearest-neighbor propensity score matching based on age, sex, race/ethnicity, income, and education. Multivariable logistic regression models were used to calculate adjusted odds ratios (ORs) for the presence of chronic inflammatory conditions. A total of 3,755 SCC cases were included (mean age 75.8; 57.0% male). After adjusting for covariates, SCC remained significantly associated with seborrheic dermatitis (OR 3.62, 95% CI [3.26—4.01]), hidradenitis suppurativa (OR 2.47 [1.24—4.76]), lichen sclerosus (OR 1.86 [1.35—2.54]), psoriasis (OR 1.64 [1.41—1.90]), rosacea (OR 2.53 [2.25—2.85]), and lichen planus (OR 2.02 [1.48—2.74]). No significant associations were observed with discoid lupus or vitiligo. These findings suggest that chronic cutaneous inflammation may play a critical role in promoting oncogenesis, potentially through mechanisms involving Th2-skewed immune responses, impaired regulatory T-cell function, and elevated levels of IL-4, IL-6, IL-10, IL-13, and TGF-β. Moreover, certain therapies used to manage inflammatory dermatoses, such as phototherapy or systemic immunosuppressants, may further contribute to carcinogenesis. These results underscore the importance of vigilant skin cancer screening in patients with inflammatory skin conditions and the need for further mechanistic and longitudinal research. 19 Synthesis and modification of Briciclib phosphonate analogs for the topical treatment of psoriasis Nicole Golob-Schwarzl1, Isabella Perchthaler1, Leo Krammer2, Alexander Wolf2, Rolf Breinbauer2,3 and Peter Wolf1,3 1 Medical University Of Graz, Department of Dermatology and Venereology, Graz, Austria, 2 Institute of Organic Chemistry, Graz University of Technology, Graz, Austria and 3 BioTechMed Graz, Graz, Austria Introduction: The systemic treatment of severe psoriasis with biologics has made considerable progress in recent decades. In contrast, little progress has been made in topical therapies for mild to moderate forms of psoriasis —affecting ∼90% of patients —highlighting the urgent need for new topical treatment options. Eukaryotic translation initiation factor 4E (eIF4E), a regulator of proliferation, apoptosis and differentiation, plays a key role in psoriasis pathogenesis. Preliminary data suggest that the eIF4E inhibitor briciclib improves the psoriatic phenotype. However, due to the hydrolytic release of a phenolic group, briciclib is not suitable for safe topical application. This necessitates the development of hydrolysis-stable, pharmacologically optimized eIF4E inhibitors for treating mild to moderate psoriasis. Methodology: We have synthesized and characterized a series of new eiF4E inhibitors to investigate the structure—activity relationships and optimize the target profiles for topical application. Selected eIF4E inhibitors were tested in vitro (HaCaT cells and skin explants) and in vivo (imiquimode) to evaluate their effects on eIf4E and its two complex partners, eIF4A and eIF4G, as well as on proinflammatory cytokines. Results: Inhibition of eIF4E reduced psoriatic inflammation both in vitro and in vivo. Downregulation of eIF4E and other eIFs by novel eIF4E inhibitors (particularly when administered topically) was associated with a normalization of cell proliferation and a reduction in psoriatic epidermal hyperplasia, as well as a normalization of levels of pro-inflammatory cytokines (e.g. TNFα, IL -1b, IL -17 and IL -22). These findings emphasize the role of eIF4E and other eIFs in the molecular pathology of the disease and highlight a translational imbalance as a potential therapeutic target. Conclusion: Our results identify eIF4E as a promising molecular target for psoriasis and support the development of safe, topically applicable eIF4E inhibitors as an innovative treatment approach for patients with mild to moderate disease. ABSTRACTS | Abstracts from the 6th Inflammatory Skin Disease Summit e34 Journal of Investigative Dermatology (2025), Volume 145

20 Systemic Biologic Treatment for Psoriasis in Elderly Patients Sapir Glazer Levavi1, Ronny Maman2, Shany Sherman1,2, Daniel Mimouni1,2 and Lev Pavlovsky1,2 1 Division Of Dermatology, Rabin Medical Center, Beilinson Hospital, Petach Tikva, Israel and 2 Faculty of Medical and Health Sciences, Tel Aviv University, Tel Aviv, Israel Approximately 3%-13% of patients with psoriasis are first affected after age 60 years. Numerous studies have investigated the use of biologic agents for the treatment of pso-riasis, but the routine exclusion of elderly adults from clinical trials has limited our knowledge about their effects in this age group. Background/Objectives: This study aimed to investigate the efficacy and safety of biologic drugs for the treatment of psoriasis in elderly patients. Methods: A single-center-based retrospective cohort study design was used. A total of 149 elderly patients with psoriasis were divided into two groups by age at initiation of biologic treatment: <65 years (adult-start group) and >65 years (elderly-start group). Data on patient characteristics were collected and analyzed, and drug survival was evaluated. Results: Demographics, comorbidities, and treatment turnover were similar in the adult-start and elderly- start groups. Drug survival of adalimumab as first-line treatment, and of guselkumab in any treatment sequence, was significantly better in the elderly-start group (p=0.029 and p=0.032, respectively). There was no be-tween-group difference in drug safety, as reflected in hospitalizations for infection or death. Conclusions: Biologic treatments for psoriasis demonstrate both efficacy and safety in elderly patients. Some agents exhibited better drug survival when initiated after age 65 years. 21 Bullous Pemphigoid as a Manifestation of Graft-Versus-Host Disease Following Allogeneic Hematopoietic Stem Cell Transplantation: A Systematic Review and Report of a Novel Case Sapir Glazer Levavi1, Moshe Yeshurun2,3, Pia Raanani2,3, Mor Frisch1, Meital Oren- Shabtai1,3, Lev Pavlovsky1,3, Daniel Mimouni1,3 and Anna Aronovich1,3 1 Division Of Dermatology, Rabin Medical Center, Beilinson Hospital, Petach Tikva, Israel, 2 Institute of Hematology, Rabin Medical Center, Beilinson Hospital, Petach Tikva, Israel and 3 Faculty of Medical and Health Sciences, Tel Aviv University, Tel Aviv, Israel Background: Bullous Pemphigoid (BP) is a well-recognized autoimmune subepidermal blistering disease. However, its occurrence following allogeneic hematopoietic stem cell transplantation (HSCT) is extremely ra-re. Objective: To systematically review the available data on BP following an allogeneic HSCT with focus on treatment options. Methods: A systematic review of studies evaluating BP following an allogeneic HSCT, in-corporating a highly treatment-resistant case from our graft-versus-host disease (GvHD) dermatology clinic, of a 47-year-old patient, notable as the only reported instance of BP following HSCT in a patient with chronic lymphocytic leukemia (CLL) that transformed into diffuse large b-cell lymphoma (DLBCL) and GvHD due to HSCT. The review yielded 15 publications that met the eligibility criteria. Including our case, a total of 16 cases were analyzed. Results: Nearly all patients (14/ 16) in this review had chronic GvHD due to their HSCT. 12 patients were males, 6 were of Japanese origin. The mean age for BP diagnosis was 38 years (rang of 5-67). On average, BP developed one year post HSCT. The most common treatment for BP in these patients was pred-nisolone, with the majority experiencing complete resolution of symptoms. Conclusion: BP following HSCT is an exceptionally rare condition with an unclear underlying mechanism. 22 Disparities in Non-Melanoma Skin Cancer Survival Among Patients with Immune-Mediated Inflammatory Diseases: A Population-Based Study Ahmed Almezaine Ministrey Of Health, Tanta, Egypt Background: Immune-mediated inflammatory diseases (IMIDs), such as psoriasis and systemic lupus erythematosus, are associated with chronic immune dysregulation and the use of immunosuppressive therapies. This immunologic environment may increase susceptibility to skin malignancies, particularly non-melanoma skin cancers (NMSCs), and influence cancer outcomes. However, population-level data on survival and disparities in this group remain limited. Objective: To evaluate overall survival and demographic disparities in NMSC patients with comorbid IMIDs using the SEER-18 database. Methods: We conducted a retrospective cohort study using SEER data (2000—2020) to identify adult patients diagnosed with either basal cell carcinoma or squamous cell carcinoma. A proxy group of IMID-associated patients was defined using treatment codes suggestive of immunosuppression, younger age at cancer diagnosis, and clinical annotation patterns. The primary outcome was 5-year overall survival (OS). Secondary analyses assessed disparities by race, sex, and geographic region. Multivariable Cox proportional hazards models were used to adjust for age, stage, tumor histology, and socioeconomic status. Results: Out of approximately 183,000 NMSC cases, 4,230 patients were classified as having probable IMID-associated disease. The 5-year OS in this group was significantly lower compared to non-IMID patients (74.6% vs. 81.2%, p <0.001). The greatest disparity was seen in African American patients with IMIDs (68.2% vs. 79.9%, adjusted HR 1.42; 95% CI 1.28—1.58). Patients from Southern U.S. regions also had poorer outcomes. IMID patients were more likely to present with high-risk histologic subtypes and advanced-stage tumors. Conclusion: Patients with immune-mediated inflammatory diseases face significantly worse survival outcomes following NMSC, particularly among racial minorities and in underserved regions. These findings highlight the need for improved surveillance, early detection, and equitable care strategies for high-risk dermatologic-oncology populations. 23 Longitudinal changes in pro-inflammatory cytokines identified by skin tape sampling in pediatric atopic dermatitis patients treated with dupilumab Elena Goleva1, Taras Lyubchenko1, Olivia Xiao1, Simion Kreimer2, Evgeny Berdyshev1, Emilie Gloaguen3, Inoncent Agueusop4, PeckY Ong5, Simon G Danby6, Michael J Cork6,7, Joseph Zahn8, Annie Zhang9 and Donald YM Leung1 1 National Jewish Health, Denver, USA, 2 Advanced Clinical Biosystems Research Institute, Cedars-Sinai Medical Center, Los Angeles, USA, 3 Sanofi, Gentilly, France, 4 Sanofi, Frankfurt, Germany, 5 Children’s Hospital Los Angeles, University of Southern California, Los Angeles, USA, 6 Sheffield Dermatology Research, University of Sheffield, Sheffield, UK, 7 Sheffield Children’s Hospital, Sheffield, UK, 8 Regeneron Pharmaceuticals, Tarrytown, USA and 9 Sanofi, Cambridge, USA This study evaluated the use of skin tape strip (STS) sampling to assess local skin pro-inflammatory cytokine production in pediatric atopic dermatitis (AD) patients during the course of 16-week dupilumab treatment and post therapy. The PEdiatric skin barrier function and LIpidomics STudy in Atopic Dermatitis (PELISTAD; NCT04718870) was an open-label study involving 6—11-year-old patients with moderate-to-severe AD. STS samples were collected from lesional and non-lesional skin of 23 AD patients and from 18 healthy volunteers over 28 weeks (16 weeks of dupilumab treatment, followed by 12 weeks off therapy). Skin cytokine levels were analyzed using Meso Scale Discovery U-Plex 20-plex cytokine assays, and results were correlated with the markers of epidermal differentiation and hyperplasia identified by mass spectrometry proteomic analysis. At baseline, lesional skin showed significantly increased pro-inflammatory cytokines IL- 1beta, IL-18, and IL-8 (p<0.0001), and decreased IL-1alpha (p<0.01). Similar trends were observed in non- lesional skin compared to healthy volunteers for these cytokines at baseline. Type 2 cytokines, including CCL17 (p<0.05), CCL22 (p=0.056), and IL-13 (p=0.19), were elevated in AD lesional skin. Dupilumab treatment led to normalization of type 2 cytokines within 2 weeks and complete suppression of IL-1beta, IL- 18, and IL-8 by week 16, with effects maintained 12 weeks post-treatment. Lesional IL-13 levels strongly correlated with IL-18 and CCL17 (p<0.0001), and with decreased expression of epidermal differentiation markers (FLG2, KRT10, ASAH1, ALOX12B, ALOXE3, SDR9C7; Spearman rho 0.58 to 0.75, p<0.01 to p<0.001). IL-13 also correlated with increased skin KRT16 expression, a hyperplasia marker. In conclusion, STS cytokine analysis revealed elevated pro-inflammatory cytokines including type 2 cytokines in pediatric AD skin. IL-13 was closely linked to impaired epidermal differentiation and increased skin hyperplasia. Longitudinal analysis demonstrated sustained suppression of local skin cytokine production with dupilumab treatment, even 12 weeks after treatment discontinuation. 24 Psoriatic fibroblasts exhibit a distinct transcriptomic profile Lili Borba´la Flink1,2, Ameneh Ghaffarinia1, Rena´ta Bozo´1,2, Dia´na Sz}ucs4, Tama´s Monostori4, Zolta´n Vere´b1,4,3, Rolland Gyulai1, Lajos Keme´ny2,3,1 and Zsuzsanna Bata-Cso¨rg}o1,2,3 1 Department Of Dermatology And Allergology, Albert Szent-gyo¨rgyi Medical School, University Of Szeged, Szeged, Hungary, 2 HCEMM-USZ Skin Research Group, University of Szeged, Szeged, Magyarorsza´g, 3 HUN-REN-SZTE Dermatological Research Group, Hungarian Research Network, Szeged, Magyarorsza´g and 4 Regenerative Medicine and Cellular Pharmacology Laboratory, Department of Dermatology and Allergology, University of Szeged, Szeged, Magyarorsza´g Psoriasis frequently recurs at previously affected sites after treatment suspension, suggesting long-lasting cellular memory in resolved lesions. Since we previously showed that keratinocytes in resolved skin retain epigenetic changes, we investigated whether fibroblasts from resolved (PS-R) psoriatic skin retain a potential inflammatory memory compared to fibroblasts from never-lesional, non-lesional (PS-NL) skin. Dermal fibroblasts were isolated from healthy (H), PS-NL, and PS-R skin of systemically treated psoriatic patients, followed by high- throughput RNA sequencing to identify differential gene expression. Reactome overrepresentation test revealed the most relevant affected pathways. In PS-NL vs. H, upregulated genes primarily affected lipid metabolism, while downregulated genes were linked to cellular stress responses and gene expression regulation. In PS-R vs. H, increased genes highlighted MAPK1/3 activation and IL-6 signaling, while decreased genes impacted cell structure and division. PS-NL vs. PS-R revealed upregulation of TP53-, NOTCH4-, and FOXO-related transcriptional pathways, with downregulation affecting ion transport, carbonic anhydrase- mediated bicarbonate production, and syndecan signaling. Our findings reveal that fibroblasts from resolved psoriatic skin exhibit distinct transcriptional profiles and functional responses compared to never-lesional fibroblasts, highlighting a retained, potential inflammatory and proliferative memory. Our findings in PS-NL fibroblasts also validate that even clinically uninvolved, never-lesional psoriatic skin exhibits subclinical alterations, which may predispose it to lesion development. 25 Endotoxemia and Psoriatic in vitro Models to Investigate Anti-inflammatory Living Therapeutic Materials Ketaki Deshpande, Varun Tadimarri and Sara Trujillo INM — Leibniz-Institut fu¨r Neue Materialien GmbH, Saarbru¨cken, Germany The most common characteristic observed in numerous diseases like rheumatoid arthritis or psoriasis is chronic inflammation. Endotoxemia is an important factor in these conditions as it is triggered by prolonged exposure to lipopolysaccharide (LPS), leading to inflammation and immune dysregulation. Therapeutic peptides are promising options to treat these chronic diseases with inflammatory characteristics. However, the applicability of therapeutic peptides is limited due to their poor stability in the body, which is typically overcome by cost-intensive modifications. Living therapeutics are emerging as a more cost-effective strategy to tackle this limitation by engineering microbes to produce and deliver the peptides right where they are needed. We developed an in-vitro endotoxemia (and psoriatic) model to test living therapeutics secreting anti-inflammatory peptides: KCF-18, I6P7, α-MSH (secreted from a genetically modified lactic acid-free strain of Lactiplantibacillus plantarum (TF103)) on murine macrophages, characterized the dose-response effects of these peptides and performed multi- array cytokine analysis. The model revealed that this living therapeutic approach enhanced the effects of the peptides, requiring lower amounts to achieve anti-inflammatory effects. Notably, α-MSH secreted by TF103 L. plantarum achieved significant pathway suppression, comparable to or exceeding that of synthetic controls, without inducing cytotoxicity. This points to potential synergistic effects between the peptides and the intrinsic anti-inflammatory properties of lactic acid bacteria. We will expand the applicability potential of these anti- inflammatory living therapeutic materials in an in vitro model of psoriasis. Abstracts from the 6th Inflammatory Skin Disease Summit | ABSTRACTS www.jidonline.org e35

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