Patients with systemic lupus erythematosus (SLE) develop anti-lymphocytotoxic antibodies (anti-LCA) measured by complement-dependent cytotoxicity assay (CDCC). In SLE, prevalence is ranging from 60 to 90% and varies according to the methods of detection and definition of test positivity. Lymphocytotoxic antibodies (LCA) have been shown to bind to several targets on lymphocytes. CD45 represent the main LCA target. Anti-ribosome P0 and antiβ2 microglobulin antibodies have been included in the spectrum of LCA. Binding to lymphocytes may vary according to the T- or B-cell subsets, to the activation state, which is the consequence of CD45 isoform variations in these cells. The pathogenic role of LCA on lymphopenia was not clearly established in vivo. Nevertheless, in vitro LCA may induce apoptosis, CDCC, and cell activation with cytokine production suggesting that LCA have the potential to influence lymphocyte functions. High titers of both IgM and IgG classes occur during phases of active nephritis and neurological lupus. Finally, LCA are reported also in quite a lot of other diseases such as Sjögren's syndrome, rheumatoid arthritis, cancer and infections. An increased incidence of LCA in consanguineous from lupus patients is described suggesting that this autoantibodies are genetically controlled.
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)