| Abstract: | Sera from patients with SLE frequently contain IgM and IgG antibodies with multiple specificities for lymphocyte surface determinants, including autologous antigens. The IgM antibodies are of relatively low binding avidity and exhibit broad reactivity with B and T lymphocytes from most individuals. IgG antibodies are reactive selectively with PBL from different individuals and appear to be more specific for B cell and a minor proportion of T cells. The molecular nature of the surface determinants involved and their relationship with known antigens and receptors remain largely undefined. Interest in anti-lymphocyte antibodies in SLE relates in part to data suggesting a causal role in the abnormal immune system function in this disorder. In this regard, possible mechanisms that are supported by indirect data include: a) antibody-mediated lymphocyte depletion in vivo, perhaps involving functional subsets specifically; b) antibody blockade of surface receptors operant in cell-cell and in cell-soluble antigen interactions. Certain data have raised the possibility that anti-lymphocyte antibodies represent serum markers for infection with virus as etiologic in SLE, but this question is controversial. Nevertheless, further investigation may yet reveal viral or genetically determined “SLE-specific” lymphocyte surface antigens. Clinically, anti-lymphocyte antibodies may have potential for mediating tissue injury in SLE, either directly or indirectly as circulating complexes in association with “shed” lymphocyte surface antigen. Direct evidence in support of such a role in the natural history of this disorder has not been forthcoming. |
