Abnormal Polyclonal B Cell Activation in NZB/NZW F1 Mice
Philip L. Cohen, Morris Ziff
Abstract
Philip L. Cohen, Morris Ziff
Abstract
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.
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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.
Key concepts: Polyclonal antibodies, Spleen, In vitro, Autoantibody, B cell, Immunology, Antibody, Suppressor