The relationship between circulating CD5+ B lymphocytes and in vitro autoantibody synthesis in normal individuals.
Recent observations suggest that a subpopulation of B lymphocytes bearing the phenotype CD5+ may be enriched for cells committed to the synthesis and secretion of autoantibodies. We had previously shown that a subset of normal individuals has an expanded subpopulation of B lymphocytes committed to the synthesis of IgM and IgM-rheumatoid factor (RF), and that this condition was associated with HLA-DR4 (4). In these studies, we performed simultaneous quantitation of the size of the circulating CD5+ B lymphocyte subpopulation in a group of 20 normal donors, and of the pokeweed mitogen-induced in vitro synthesis of a panel of autoantibodies by the same peripheral blood cells depleted of CD8+ suppressor lymphocytes in 18 of the 20 individuals. The culture supernatants were assayed for total IgM and IgG, RF, IgM, and IgG anti-single-stranded DNA, anti-human thyroglobulin, and anti-tetanus toxoid. The mean percentage CD5+ B cells was 13.5 +/- 2.5%. There was no significant correlation between total B lymphocytes and CD5+ B cells (R = 0.25, P greater than 0.20. Positive correlations were found between the proportion of circulating CD5+ B lymphocytes and synthesis of RF (R = 0.73, P less than 0.001), and IgM anti-DNA (R = 0.58, P less than 0.03). Significant correlations were not found between CD5+ B cells and secreted IgM or IgG antibodies against the exogenous antigen tetanus toxoid, measured in the same supernatants. The antibodies produced in vitro by T cell-dependent B cell activation appear to have limited or no polyspecificity. These results indicate that the size of the circulating CD5+ B cell subpopulation in any given individual contributes importantly to the magnitude of autoantibody synthesis in cultures where T cell-mediated B lymphocyte activation takes place in the absence of suppressor signals.
Jasin
H E
HE
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.
D015703:Antigens, CD / Q000032:analysis*; D000943:Antigens, Differentiation / Q000032:analysis*; D001323:Autoantibodies / Q000096:biosynthesis*; D001402:B-Lymphocytes / Q000276:immunology*; D018956:CD5 Antigens; D006801:Humans; D007074:Immunoglobulin G / Q000096:biosynthesis; D007075:Immunoglobulin M / Q000096:biosynthesis; D012217:Rheumatoid Factor / Q000096:biosynthesis
D015703:Antigens, CD; D000943:Antigens, Differentiation; D001323:Autoantibodies; D018956:CD5 Antigens; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D012217:Rheumatoid Factor