Abnormal polyclonal B cell activation in NZB/NZW F1 mice.
Spleen cells from autoimmune (10-mont-old) NZB/NZW (B/W) mice failed to generate appreciable numbers of antibody-forming cells (AFC) in vitro to TNP-substituted sheep erythrocytes in response to the polyclonal B cell activators (PBA), LPS and PPD, despite normal DNA synthetic responses to these agents and normal AFC responses to TNP-Ficoll. The failure to respond to PBA in old B/W mice was not due to suppressor T cells since anti-brain-associated-theta-treated spleen cells still failed to generate AFC in response to PBA. The defect was age-related since cells from young B/W mice generated vigorous AFC responses to PBA. It is suggested that the failure of the spleen cells of old B/W mice to generate AFC is a result of in vitro polyclonal B cell activation in the course of autoantibody formation.
D000375:Aging; D000818:Animals; D000917:Antibody Formation; D000921:Antibody-Producing Cells; D001323:Autoantibodies; D001921:Brain; D004247:DNA / Q000096:biosynthesis; D007106:Immune Sera; D037102:Lectins; D008070:Lipopolysaccharides / Q000276:immunology; D051379:Mice; D008814:Mice, Inbred NZB / Q000276:immunology*; D013154:Spleen / Q000166:cytology; D014301:Trinitrobenzenes / Q000276:immunology; D014373:Tuberculin
D001323:Autoantibodies; D007106:Immune Sera; D037102:Lectins; D008070:Lipopolysaccharides; D014301:Trinitrobenzenes; D014373:Tuberculin; D004247:DNA