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.