Identification of Clec4b as a novel regulator of bystander activation of auto-reactive T cells and autoimmune disease

• DOI: 10.1371/journal.pgen.1008788
• Publication Date: 2020-06-04T17:53:05Z
• Authors: Liselotte Bäckdahl; Mike Aoun; Ulrika Norin; Rikard Holmdahl
• Keywords: Bystander effect

The control of chronic inflammation is dependent on the possibility limiting bystander activation autoreactive and potentially pathogenic T cells. We have identified a non-sense loss function single nucleotide polymorphism in C-type lectin receptor, Clec4b, shown that it controls autoimmune arthritis rat models rheumatoid arthritis. Clec4b specifically expressed CD4+ myeloid cells, mainly classical dendritic cells (DCs), defined by markers CD4+/MHCIIhi/CD11b/c+. found limited arthritogenic CD4+αβT absence allowed development already 5 days after adjuvant injection. sufficient successfully cell expansion immediately both vitro vivo. conclude regulate auto-reactive during an immune response, demonstrating early checkpoint mechanism to avoid autoimmunity leading inflammation.