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pubmed:abstractText |
As has been found for spleen cells from ageing NZB x NZW (B/W) mice, ageing NZB mice were also found to make no antibody when stimulated in vitro with the polyclonal B cell activators (PBA) LPS and PPD. This immune defect was not due to the action of suppressor cells, since old NZB and B/W spleen cells did not suppress the PBA response of young spleen cells. Spleen cells from aged NZB mice were not able to generate antibody-forming cells when stimulated with the thymus-independent antigen, TNP-LPS, but were able to produce antibody in response to another thymus-independent antigen, TNP-AECM-Ficoll, thereby implying that there is a selective functional deletion of a B cell subpopulation in ageing New Zealand mice. The failure of B/W and NZB spleen cells to generate antibody in response to PBA is interpreted as a consequence of a continuing in vivo polyclonal B cell activation accompanying the development of autoimmune disease, leading to a scarcity of B cells available for activation by PBA and by some thymus-independent antigens in vitro.
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