Abstract
Abstract Aging New Zealand mice develop impaired cellular immune functions including delayed rejection of primary skin allografts, a model of cellular immunity. In the first paper in this series it was found that old NZB/W mice are deficient in a recirculating T cell subpopulation which is present in young NZB/W mice. This T cell synergizes with a second T cell subpopulation present in both young and old NZB/W mice to effect prompt allograft rejection. The present study investigates the mechanism by which recirculating T cells cooperating in skin allograft rejection are eliminated as New Zealand mice age. It was found that a host factor diverts lymphoid cells from the recirculating pool. This host factor was found to have specificity for an antigen common to thymocyte and brain suggesting that it was similar to antisera to the Thy 1 (θ) antigen; the naturally occurring antithymocyte antibody (NTA) present in New Zealand mice has the same type of specificity. It appears that NTA leads to a reduction in recirculating T cells as New Zealand mice age resulting in impaired cellular immunity.
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