Antibodies to T cells in patients with systemic lupus erythematosus can induce antibody-dependent cell-mediated cytotoxicity against human T cells.
Patients with active systemic lupus erythematosus (SLE) often have circulating antibodies to T cells. These patients also often have leukopenia and diminished numbers of T lymphocytes. In addition, certain T lymphocyte functions are frequently impaired in patients with SLE. It has been previously considered that a complement-dependent cytotoxic mechanism was responsible for the above observations. We now demonstrate that antibody-dependent cell-mediated cytotoxicity (ADCC), a cytotoxic reaction mediated by antibody and effector cells in the absence of complement, can also kill T cells from normal individuals as well as from patients with SLE. Moreover, this ADCC could be observed using the plasma, effector cells, and target cells all obtained from the same individual with SLE. Plasma of those patients with active SLE, and in whom anti-T cell antibodies could be demonstrated by the more classical complement-dependent cytotoxicity, was most often able to mediate such an ADCC reaction. The IgG fraction of the plasma was responsible for inducing ADCC, and aggregated IgG could block the reaction. The fact that the IgG fraction was often more effective than the unfractionated plasma suggested that immune complexes present in SLE plasma might partially block the expression of ADCC. Because a single SLE plasma could induce ADCC in T cells from several different unrelated individuals, it is unlikely that antibodies directed against particular human leukocyte antigens (HLA) or blood group antigens are involved.
D000920:Antibody-Dependent Cell Cytotoxicity; D002478:Cells, Cultured; D003165:Complement System Proteins / Q000276:immunology; D006801:Humans; D007111:Immunity, Cellular; D007518:Isoantibodies; D008180:Lupus Erythematosus, Systemic / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*
D007518:Isoantibodies; D003165:Complement System Proteins