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

Monoclonal anti-beta 2-microglobulin (beta 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-beta 2m exhibited effects similar to those of sera from patients with SLE. Although 10 of 16 SLE sera contained antibody to beta 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-beta 2m from SLE serum by solid phase absorption with beta 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-beta 2m) nor heterologous anti-beta 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 beta 2m, the E receptor, and T-cell activation. While anti-beta 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.