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INTERLEUKIN‐1 AND INTERLEUKIN‐2 DEFECTS ASSOCIATED WITH MURINE GRAFT‐VERSUS‐HOST‐INDUCED IMMUNODEFICIENCY

In this study we investigated the mechanism, or mechanisms, involved in graft-versus-host (GVH)-induced T cell immunodeficiency. Chronic GVH reactions were induced in normal CBAxA F1 (BAF1) hybrid mice by the injection of parental A strain lymphoid cells. At various times (43–91 days) after GVH induction, the functional status of GVH T cells was assessed using interleukin-1 (IL-1) and interleukin-2 (IL-2) as probes. The response of GVH thymocytes to IL-1 was depressed when compared with normal thymocytes. Although GVH peanut-agglutinin-negative (PNA-) thymocytes did respond to IL-2 alone or IL-2 plus phytohemagglutinin (PHA), this response was significantly lower than the response of PNA- thymocytes from normal mice. In addition, GVH spleen cells failed to produce significant amounts of IL-2 when stimulated with concanavalin A. These results suggest that the long term immunosuppression associated with murine chronic GVH disease is due, at least in part, to a decrease in the responsiveness to IL-1 and IL-2, and to a marked deficiency in IL-2 production.