PhD Scientific Days 2023

Molecular Sciences IV.

The role of Dectin-2 in the development of antibody-induced experimental dermatitis

Előadó neve

Balogh, Lili

Neptun code

CMGK6E

Előadó munkahelye

Semmelweis Universitiy, Department of Physiology

Előadó telefonszáma

06203710374

Előadó e-mail címe

balogh.lili@stud.semmelweis.hu

Az előadás címe

The role of Dectin-2 in the development of antibody-induced experimental dermatitis

Szerző(k) neve és munkahelye

Lili Balogh1,2, Silvia Hayer3, Stephan Blüml3, Attila Mócsai1 and Tamás Németh1,2,4
1Department of Physiology, Semmelweis University, Budapest, Hungary
2MTA-SE “Lendület” Translational Rheumatology Research Group, Hungarian Academy of Sciences and Semmelweis University, Budapest, Hungary
3Department of Rheumatology, Medical University of Vienna, Vienna, Austria
4Department of Rheumatology and Clinical Immunology, Semmelweis University, Budapest, Hungary

Bemutatás módja

Szóbeli

Szekció

Molecular Sciences IV.

Language of the presentation

Hungarian

Preferred session

Health Sciences

Összefoglaló szövege

Introduction: The C-type lectin receptor Dectin-2 is essential for antimicrobial processes and it is expressed in various immune cells. Polymorphisms of the gene of Dectin-2 have been associated with rheumatoid arthritis, while we found that the expression of Dectin-2 increased in immune complex-activated neutrophils. These findings raised the possibility that Dectin-2 might have a role in immune complex-mediated diseases, such as epidermolysis bullosa acquisita (EBA), an autoimmune blistering disease, where autoantibodies against type VII collagen lead to dermo-epidermal separation.
Aim: Our aim was to test the role of Dectin-2 in an in vivo experimental model of EBA.
Methods: We used wild type and Dectin-2 knock out (Clec4n―/―) mice. The passive form of EBA was triggered by repeated injections of anti-type VII collagen antibodies. Disease progression was followed by clinical assessment and quantitative scoring. Histological slides were stained with H&E, and the antibody-deposition was detected by direct immunofluorescence. In vivo neutrophil accumulation was measured by flow cytometry and local CXCL2 chemokine levels were detected by ELISA. In our in vitro experiments, neutrophils were activated by immune complexes, their superoxide release was followed by a cytochrome c reduction test, while their cell spreading was measured by a phase-contrast microscope.
Results: The development of experimental EBA was dramatically reduced in the Dectin-2 KO mice compared to wild type animals, while the antibody-deposition did not differ in the two genotypes. The in vivo neutrophil recruitment and CXCL2 levels were also massively reduced in the knockouts. Meanwhile, the immune complex-stimulated Dectin-2 KO neutrophils produced smaller amounts of superoxide and showed reduced cell spreading in contrast to wild type cells.
Conclusion: Our results indicate that Dectin-2 is needed for the proper development of antibody-induced dermatitis, probably due to its role in immune complex-mediated neutrophil functions. These findings can lead to a better understanding of the pathogenesis of autoimmune blistering skin diseases and may help to develop new therapies in the future.
Funding: This work was supported by the Hungarian National Research, Development and Innovation Office.

University and Doctoral School

Semmelweis University, Doctoral School of Molecular Medicine

Supervisor

Dr. Németh Tamás

Publication of my abstract

I do not give consent to the publication of my abstract on the website of the congress.

Kind

Szabad

Status

elfogadva

Accepted presentation method

szóbeli

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

7444

Start

16:15

End

16:30

Authors (legacy)

Lili Balogh1,2, Silvia Hayer3, Stephan Blüml3, Attila Mócsai1 and Tamás Németh1,2,4
1Department of Physiology, Semmelweis University, Budapest, Hungary
2MTA-SE “Lendület” Translational Rheumatology Research Group, Hungarian Academy of Sciences and Semmelweis University, Budapest, Hungary
3Department of Rheumatology, Medical University of Vienna, Vienna, Austria
4Department of Rheumatology and Clinical Immunology, Semmelweis University, Budapest, Hungary