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Peer-reviewedCC BY 4.0Frontiers in Immunology

The C-type lectin receptor Dectin-2 is crucial for the development of experimental autoimmune skin disease

  • Lili Balogh1,2
  • Eszter Káposztás1,2
  • Tamara Józsa1,2
  • Viktor Gyula Kovács1,2
  • Silvia Hayer3,4
  • Stephan Blüml3
  • Attila Mócsai1,5,6
  • Tamás Németh1,2,7
7 affiliations
  1. 1Department of Physiology, Semmelweis University School of Medicine
  2. 2MTA-SE “Lendület” Translational Rheumatology Research Group, Hungarian Academy of Sciences and Semmelweis University
  3. 3Department of Internal Medicine III, Division of Rheumatology, Medical University of Vienna
  4. 4Ludwig Boltzmann Institute for Arthritis and Rehabilitation
  5. 5HUN-REN-SE Inflammation Physiology Research Group, HUN-REN Hungarian Research Network and Semmelweis University
  6. 6MTA-SE “Lendület” Inflammation Physiology Research Group, Hungarian Academy of Sciences and Semmelweis University
  7. 7Department of Rheumatology and Immunology, Semmelweis University
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Abstract

Autoimmune blistering skin diseases have deleterious effects on patients’ lives with a great (and unmet) need for more treatment options and potential new drug targets. C-type lectin receptors like Dectin-2 are pattern recognition receptors that bind to carbohydrate moieties on microorganisms leading to the elimination of the pathogens. Recently, Dectin-2 gene variants have been linked to autoimmune diseases, its expression in neutrophils has been shown to be upregulated in the autoimmune blistering skin disease epidermolysis bullosa acquisita (EBA), while we found that immune complex-stimulated neutrophils upregulated the gene of Dectin-2. These results prompted us to test the role of Dectin-2 in neutrophil- and autoantibody-mediated experimental inflammation. Dectin-2-deficient mice showed a nearly complete protection against the development of EBA, which was further validated in the reverse passive Arthus reaction. Immune cell accumulation and proinflammatory mediator levels were also decreased in Dectin-2 –/– mice. In line with these findings, postmigratory Fc receptor-dependent neutrophil, but not macrophage functions were dramatically reduced in the absence of Dectin-2. Our results show an essential role for Dectin-2 in immune complex-mediated in vitro neutrophil processes, in experimental EBA and immune complex-mediated inflammation, which raise the possibility that this C-type lectin receptor could be a treatment target in these disorders.

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Cite

BibTeXRIS
BibTeX
@article{balogh2026ctype,
  title = {{The C-type lectin receptor Dectin-2 is crucial for the development of experimental autoimmune skin disease}},
  author = {Lili Balogh and Eszter Káposztás and Tamara Józsa and Viktor Gyula Kovács and Silvia Hayer and Stephan Blüml and Attila Mócsai and Tamás Németh},
  journal = {Frontiers in Immunology},
  year = {2026},
  month = oct,
  doi = {10.3389/fimmu.2026.1962664},
  url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1962664/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - The C-type lectin receptor Dectin-2 is crucial for the development of experimental autoimmune skin disease
AU  - Lili Balogh
AU  - Eszter Káposztás
AU  - Tamara Józsa
AU  - Viktor Gyula Kovács
AU  - Silvia Hayer
AU  - Stephan Blüml
AU  - Attila Mócsai
AU  - Tamás Németh
PY  - 2026
DA  - 2026/10/28
JO  - Frontiers in Immunology
DO  - 10.3389/fimmu.2026.1962664
UR  - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1962664/full
AB  - Autoimmune blistering skin diseases have deleterious effects on patients’ lives with a great (and unmet) need for more treatment options and potential new drug targets. C-type lectin receptors like Dectin-2 are pattern recognition receptors that bind to carbohydrate moieties on microorganisms leading to the elimination of the pathogens. Recently, Dectin-2 gene variants have been linked to autoimmune diseases, its expression in neutrophils has been shown to be upregulated in the autoimmune blistering skin disease epidermolysis bullosa acquisita (EBA), while we found that immune complex-stimulated neutrophils upregulated the gene of Dectin-2. These results prompted us to test the role of Dectin-2 in neutrophil- and autoantibody-mediated experimental inflammation. Dectin-2-deficient mice showed a nearly complete protection against the development of EBA, which was further validated in the reverse passive Arthus reaction. Immune cell accumulation and proinflammatory mediator levels were also decreased in Dectin-2 –/– mice. In line with these findings, postmigratory Fc receptor-dependent neutrophil, but not macrophage functions were dramatically reduced in the absence of Dectin-2. Our results show an essential role for Dectin-2 in immune complex-mediated in vitro neutrophil processes, in experimental EBA and immune complex-mediated inflammation, which raise the possibility that this C-type lectin receptor could be a treatment target in these disorders.
SN  - 1664-3224
ER  -