Increased responsiveness of rheumatoid B lymphocytes to stimulation by Epstein-Barr virus.
Blood lymphocytes from rheumatoid patients and normal subjects were examined for responsiveness in culture to Epstein-Barr virus (EBV) infection by outgrowth assay and 3HTdR uptake. With both unseparated and B-cell-enriched lymphocytes the frequency and rate of outgrowth to form permanent cell lines were significantly higher for rheumatoid than for normal cells. In B-enriched rheumatoid preparations the proportion of responsive cells was also greater, and DNA synthesis was induced by a lower infecting dose of EBV in rheumatoid than in normal cells. The percentage of autologous T cells needed to ensure regression of B-cell proliferation in EBV-infected cultures was considerably higher with rheumatoid than with normal cells. These findings suggest that in rheumatoid arthritis the abnormal lymphocyte responsiveness to EBV has two components, a T-cell immunoregulatory defect, and a separate increased responsiveness of B cells to EBV.
D000911:Antibodies, Monoclonal / Q000276:immunology; D001172:Arthritis, Rheumatoid / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology*; D004854:Herpesvirus 4, Human / Q000276:immunology*; D006801:Humans; D008213:Lymphocyte Activation; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D013936:Thymidine / Q000378:metabolism
D000911:Antibodies, Monoclonal; D013936:Thymidine