Relationship of anti-β 2-microglobulin antibodies to T11 and T-cell activation in systemic lupus erythematosus

Abstract

Monoclonal anti-β 2-microglobulin (β 2m) inhibited in a specific, dose-dependent fashion both in vitro tetanus toxoid-induced human-T-cell proliferation and sheep erythrocyte (E)-rosette formation, a function of the 50 kDa T11 molecule. In these respects, anti-β 2m exhibited effects similar to those of sera from patients with SLE. Although 10 of 16 SLE sera contained antibody to β 2m in monoclonal rosette inhibition assays, the presence of antibody of this specificity contributed only partially to the capacity of SLE serum to inhibit E-rosette formation or the T-cell response to tetanus toxoid. Removal of anti-β 2m from SLE serum by solid phase absorption with β 2m-Sepharose 4B reduced inhibition of the tetanus toxoid response and E-rosette formation in certain cases, but to a lesser extent than that observed following absorption with T-cell blasts, which completely eliminated inhibitory activity. Neither SLE antilymphocyte antibodies (including anti-β 2m) nor heterologous anti-β 2m were directed to the E receptor binding site (T11 1 epitope), as indicated by failure to inhibit OKT11 monoclonal antibody rosette formation or to reduce the relative intensity of OKT11 immunofluorescent staining. These data suggest an interesting functional relationship between β 2m, the E receptor, and T-cell activation. While anti-β 2m antibodies in SLE exert some inhibitory effect on antigen-induced T-cell proliferation, other distinct autoantibody systems to T-cell activation antigens appear to play the predominant role in this regard.