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Identification of Clec4b as a novel regulator of bystander activation of auto-reactive T cells and autoimmune disease.
- Source :
-
PLoS genetics [PLoS Genet] 2020 Jun 04; Vol. 16 (6), pp. e1008788. Date of Electronic Publication: 2020 Jun 04 (Print Publication: 2020). - Publication Year :
- 2020
-
Abstract
- The control of chronic inflammation is dependent on the possibility of limiting bystander activation of autoreactive and potentially pathogenic T cells. We have identified a non-sense loss of function single nucleotide polymorphism in the C-type lectin receptor, Clec4b, and have shown that it controls chronic autoimmune arthritis in rat models of rheumatoid arthritis. Clec4b is specifically expressed in CD4+ myeloid cells, mainly classical dendritic cells (DCs), and is defined by the markers CD4+/MHCIIhi/CD11b/c+. We found that Clec4b limited the activation of arthritogenic CD4+αβT cells and the absence of Clec4b allowed development of arthritis already 5 days after adjuvant injection. Clec4b sufficient CD4+ myeloid dendritic cells successfully limited the arthritogenic T cell expansion immediately after activation both in vitro and in vivo. We conclude that Clec4b expressed on CD4+ myeloid dendritic cells regulate the expansion of auto-reactive and potentially pathogenic T cells during an immune response, demonstrating an early checkpoint control mechanism to avoid autoimmunity leading to chronic inflammation.<br />Competing Interests: The authors have declared that no competing interests exist.
Details
- Language :
- English
- ISSN :
- 1553-7404
- Volume :
- 16
- Issue :
- 6
- Database :
- MEDLINE
- Journal :
- PLoS genetics
- Publication Type :
- Academic Journal
- Accession number :
- 32497089
- Full Text :
- https://doi.org/10.1371/journal.pgen.1008788