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TL;DR
This preclinical mouse study found that autoreactive B cells specific to collagen type II can activate regulatory T cells and suppress autoimmune arthritis, suggesting a natural tolerizing mechanism.
The Journal of Experimental Medicine · 25 authors, 12 centres
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This preclinical mouse study found that autoreactive B cells specific to collagen type II can activate regulatory T cells and suppress autoimmune arthritis, suggesting a natural tolerizing mechanism.
The study used mouse models, including collagen-induced arthritis and ACB.Col2R360Q knock-in mice, to investigate autoreactive B cells specific for collagen type II (C1-B). Researchers identified a population of these B cells in the natural repertoire that escapes negative selection. Central findings show that C1-B cells can activate collagen-specific regulatory T cells (Tregs) and suppress autoimmune arthritis in vivo. Mechanistic experiments implicated the surface protein CD72 in mediating this suppressive function. The study also found that the frequency of C1-B cells is decreased in human rheumatoid arthritis patients. The implications suggest a physiological role for certain autoreactive B cells in maintaining immune tolerance and potentially offering new avenues for autoimmune therapy.