PhD Scientific Days 2026

Poster Session 1.S - Conservative Medicine

Exploring Therapeutic Targets in Bullous Pemphigoid: Effects on Ex Vivo Blister Formation

Előadó neve

Ms. Sodbuyan, Enkhbilguun, MSc

Neptune code

JN19B9

Előadó munkahelye

Semmelweis University

Előadó telefonszáma

+36205918727

Előadó e-mail címe

enkhbilguun.sodbuyan@phd.semmelweis.hu

Az előadás címe

Exploring Therapeutic Targets in Bullous Pemphigoid: Effects on Ex Vivo Blister Formation

Szerző(k) neve és munkahelye

Enkhbilguun Sodbuyan¹

1: Semmelweis University

Bemutatás módja

Poszter

Szekció

Poster Session 1.S - Conservative Medicine

Language of the presentation

English

Preferred session

Conservative Medicine

Összefoglaló szövege

Introduction: Bullous pemphigoid (BP) is an autoimmune blistering skin disorder characterized 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 granulocyte recruitment, leading to DEJ degradation and blister formation. Although glucocorticoids remain first-line therapy, refractory cases require additional immunosuppressants or biologic treatments.
Aim: This study aimed to explore therapeutic strategies by evaluating a selection of clinically available drugs, each with distinct mechanisms of action: infliximab (TNF-α inhibitor), mepolizumab and nemolizumab (type-2 inflammation-related inhibitors); upadacitinib and baricitinib (JAK inhibitors); C1 esterase inhibitor, ravulizumab and pegcetacoplan (complement inhibitors); and TIMP-1 and IL-10 (endogenous regulators).
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: Pretreatment of PMNs with JAK inhibitors, C3 and C5 complement inhibitors resulted in the strongest inhibition of DEJ separation. Infliximab also significantly reduced DEJ separation in a dose-dependent manner. In contrast, type-2 inflammation-related inhibitors have shown inconsistent or insignificant effects.
Conclusion: These findings suggest that C3 and C5 complement inhibitors, as well as JAK inhibitors and infliximab, may directly inhibit PMN mediated blister formation in BP. Targeting cytokine signaling and complement pathways may offer promising steroid sparing and more precise therapeutic options. The limited efficacy of type 2 inflammation–related inhibitors may reflect the fact that their mechanisms operate through pathways not captured in this ex vivo model.
Funding: The research was funded by the Hungarian National Research, Development and Innovation Office (TKP2021-EGA-29) and Semmelweis 250+ Excellence Scholarship.

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

16:54

End

16:57