Figure 7.

Distinct roles of different β2 microglobulin (β2m)-associated glycoproteins in the regulation of humoral autoimmunity. The findings in this report and previous studies suggest that β2m may affect lupus-like autoimmunity via at least six possible mechanisms: 1) neonatal Fc receptor (FcRn) effects on immunoglobulin G (IgG) catabolism [17,18] (Figure 2); 2) Qa-1-restricted CD8+ regulatory or suppressor T-cells that can suppress autoimmunity [39]; 3) major histocompatability complex (MHC) class I-restricted CD8+ Ti cells (inhibitory T-cells) that suppress autoantibody production via production of transforming growth factor β [5,28]; 4) MHC class I-restricted CD8+ cytotoxic T lymphocytes (CTL) that can ablate autoreactive B-cells [6]; 5) protective role of CD1d-restricted glycolipid (GL)-reactive invariant natural killer T (iNKT)-cells in autoimmunity [8,24,31,42,44] (Figures 4 and 6a); and 6) the ability of CD1d to bind phospholipid (PL) antigens to induce anti-phospholipid autoimmunity (Figure 5). RF, rheumatoid factor; APC, antigen presenting cell.

Singh et al. Arthritis Research & Therapy 2013 15:R47   doi:10.1186/ar4206
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