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Type II collagen-specific T cells are a subset of CD4+ T lymphocytes that recognize epitopes derived from type II collagen (CII), the main protein component of cartilage. These cells play a central role in the pathogenesis of autoimmune diseases such as rheumatoid arthritis (RA) and in animal models like collagen-induced arthritis (CIA). Their activation depends on recognition of post-translationally modified epitopes presented by specific MHC class II molecules. While tightly regulated under normal conditions through peripheral tolerance mechanisms, loss or bypassing of this control leads to their expansion and effector function—driving chronic inflammation characteristic of RA. Therapeutic strategies targeting these pathways aim either at restoring tolerance or selectively modulating their activity for disease amelioration.
Induction of Col II-specific regulatory T-cells (Tregs) that migrate into inflamed joints and suppress local inflammation
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