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

Name of the presenter

Balogh, Lili

Institute/workplace of the presenter

Department of Physiology, Semmelweis University

Authors

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

Text of the abstract

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.