PhD Scientific Days 2025
Budapest, 7-9 July 2025
Poster Session III. - X: Conservative Medicine
Effect of Pathogenic Component Inhibition on Bullous Pemphigoid
Előadó neve
Ms. Sodbuyan Enkhbilguun, MSc
Neptun code
JN19B9
Előadó munkahelye
Semmelweis University
Előadó telefonszáma
+36205918727
Előadó e-mail címe
enkhbilguun.sodbuyan@phd.semmelweis.hu
Az előadás címe
Effect of Pathogenic Component Inhibition on Bullous Pemphigoid
Szerző(k) neve és munkahelye
Enkhbilguun Sodbuyan1, Prof. Dr. Sárdy Miklós2
1: Károly Rácz Conservative Medicine Division, Doctoral College, Semmelweis University
2: Department of Dermatology, Venereology and Dermatooncology, Semmelweis University
Bemutatás módja
Poszter
Szekció
Poster Session III. - X: Conservative Medicine
Language of the presentation
English
Preferred session
Conservative Medicine
Összefoglaló szövege
Introduction: Bullous pemphigoid (BP) is an autoimmune blistering skin disorder characterised by IgG and IgE autoantibodies targeting structural proteins, collagen XVII (BP180) and dystonin-e (BP230), at the dermal-epidermal junction (DEJ). Autoantibody binding triggers immune complex formation, complement activation, and recruitment of granulocytes, leading to DEJ degradation and blister formation. While glucocorticoids remain first-line therapy, refractory cases require additional immunosuppressants or biologics.
Aim: To explore therapeutic strategies by evaluating a selection of clinically available drugs, each with a distinct mechanism of actions: methylprednisolone (glucocorticoid), dapsone (neutrophil-inhibiting antibiotic), infliximab (TNF-α inhibitor), dupilumab (IL-4 and IL-13 inhibitor), omalizumab (IgE inhibitor) and intravenous immunoglobulin (IVIg, immunomodulator).
Methods: In this pilot study, we evaluated the effects of the aforementioned drugs on blister formation in BP using an ex vivo skin separation model of BP, where human skin sections were incubated with BP sera and polymorphonuclear neutrophils (PMNs).
Results: Pretreatments of PMNs with methylprednisolone, infliximab, and dupilumab significantly reduced DEJ separation, with methylprednisolone and infliximab showing the strongest dose-dependent inhibition. In contrast, dapsone, IVIg and omalizumab treatments did not have significant effects on the blister formation.
Conclusion: These findings suggest that methylprednisolone, infliximab, and dupilumab can directly inhibit PMN-mediated blister formation in BP. Targeting cytokine and signal transduction pathways may offer promising steroid-sparing and more precise therapeutic options. The lack of efficacy with dapsone, omalizumab and IVIg treatments can be due to their mechanisms operating through pathways not captured here. Future experiments investigating more targeted inhibitors can help identify additional therapeutic options necessary for developing personalised treatment strategies and improving outcomes for BP patients.
Funding: The research was funded by the Hungarian National Research, Development and Innovation Office (TKP2021-EGA-29).
University
Semmelweis University
Supervisor
Prof. Dr. Sárdy Miklós
Publication of my abstract
I do not give consent to the publication of my abstract on the website of the congress.
phd.section.field
in doctoral studies after complex exam (PhD)
Kind
Szabad
Status
elfogadva
Accepted presentation method
poszter
Előadás fájl jóváhagyás
nem rendelkezett róla
Előadó
9148
Start
14:30
End
14:36