PhD Scientific Days 2026

Poster Session 1.A - Molecular Medicine

The role of a C-type lectin receptor in immune complex-mediated cell responses of phagocytes

Előadó neve

Dr. Balogh, Lili

Neptune code

CMGK6E

Előadó munkahelye

Department of Physiology, Semmelweis University

Előadó telefonszáma

+36 1 459 1500 / 60334

Előadó e-mail címe

balogh.lili@semmelweis.hu

Az előadás címe

The role of a C-type lectin receptor in immune complex-mediated cell responses of phagocytes

Szerző(k) neve és munkahelye

Lili Balogh¹, Eszter Káposztás², Viktor Gyula Kovács², Silvia Hayer³, Stephan Blüml³, Attila Mócsai², Tamás Németh²

1: Department of Physiology, Semmelweis University
2: Department of Physiology, Semmelweis University, Budapest, Hungary
3: Department of Internal Medicine III, Division of Rheumatology, Medical University of Vienna, Vienna, Austria

Bemutatás módja

Poszter

Szekció

Poster Session 1.A - Molecular Medicine

Language of the presentation

English

Preferred session

Molecular Medicine

Összefoglaló szövege

I: Among other C-type lectin receptors, the expression of Dectin-2 showed upregulation in (experimental) immune complex-mediated epidermolysis bullosa acquisita (EBA). In line with this finding, we have found that Dectin-2 knockout (Dectin-2‒/‒) mice were almost completely protected against experimental EBA, where the accumulation of neutrophils and macrophages at the site of inflammation were dramatically decreased in Dectin-2‒/‒ mice compared to wild type animals.
A: Here, we investigated which phagocytes require Dectin-2 expression for their in vitro cell responses.
M: We used wild type and Dectin-2‒/‒ mice. Peripheral and bone marrow neutrophil and macrophage counts and cell surface expression of crucial receptors were measured by flow cytometry. Freshly isolated mouse neutrophils or cultured bone marrow-derived macrophages were activated by immune complex surfaces in vitro. Superoxide release of neutrophils was measured by a cytochrome c reduction test, while production of reactive oxygen species by macrophages was detected by a chemiluminescence method. In vitro cytokine levels were measured by ELISA. Neutrophil migration was tested in the in vitro Transwell assay.
R: The absence of Dectin-2 did not affect the bone marrow or the circulating phagocyte cell numbers. The maturation and the expression of cell surface markers (e.g. Fc receptors, integrins) were unaffected by Dectin-2-deficiency. Immune complex-activated Dectin-2‒/‒ neutrophils showed significantly decreased superoxide and cytokine release in contrast to wild type cells, while their in vitro migration was not impaired. On the other hand, immune-complex-mediated cell responses of Dectin-2‒/‒ macrophages were comparable to wild type cells.
C: Our results indicate that the essential role of Dectin-2 in the development of autoimmune dermatitis is probably due to the importance of this receptor in immune complex-mediated neutrophil functions. Our findings help us to better understand the pathomechanism of Fc receptor-mediated autoimmune skin diseases, while Dectin-2 may serve as a potential therapeutic target in these disorders in the future.
F: This work was funded and supported by the Hungarian National Research, Development and Innovation Office (Grant number: ANN 139112 to T.N.). Lili Balogh is a recipient of an SE 250+ Excellence PhD Scholarship.

University

Semmelweis University

Supervisor

Dr. Tamás Németh

Publication of my abstract

I 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

7444

Start

16:36

End

16:39