Antibodies to CD45 and other cell membrane antigens in systemic lupus erythematosus.

Abstract

At some point in their illness, most patients with systemic lupus erythematosus (SLE) develop cold-reactive IgM anti-lymphocyte autoantibodies, which appear to represent a type of natural autoantibody that exhibits a disease-related increase in titer. Increased levels of such autoantibodies are found during flares of SLE disease activity in association with lymphopenia [7, 61], suggesting a causal relationship with T cell depletion and various functional abnormalities of T cells, B cells, and monocytes. Addition of SLE serum or immunoglobulin with anti-lymphocyte autoantibody activity to in vitro cultures of normal peripheral blood mononuclear cells alters their function in ways closely paralleling that of freshly isolated lymphocytes and monocytes from patients with SLE. Mechanisms by which such functional effects could occur in vivo include: (a) elimination of cells by complement-mediated lysis, antibody-dependent, cell-mediated cytotoxicity [15], and/or opsonization; (b) alteration of lymphocyte migration patterns; (c) modulation of surface determinants [63]; (d) agonist, partial agonist, or antagonist effects on cell surface receptors [38, 39, 65]; and (e) interaction with soluble products of activated cells [18]. Thus, autoantibodies to lymphocyte and monocyte surface determinants may constitute one of the pathogenetically significant extrinsic elements that alters cellular immune function in this disorder.