The heritability of adjuvant‐induced arthritis in rats of the DA and Fisher 344 strains was examined. Development of arthritic lesions in response to a single injection of supplemented Freund's complete adjuvant has been found to be controlled by an autosomal, dominant gene locus, Ar. The capacity to respond was present in DA rats and absent in our Fisher rats. Ar has been found to be linked to the major histocompatibility complex genes with which it exhibits a high rate of recombination.

No abstract

The participation of two subpopulations of suppressor T cells (Ts) active in the suppression of hapten-specific contact sensitivity (CS) was investigated in the down-regulation of in vivo development of CTL to hapten-altered self. We have shown that Ts efferent (Ts-eff) cell that is induced by tolerizing mice with an i.v. injection of hapten-coupled syngeneic spleen cells, and the auxiliary Ts cell (Ts-aux), which is generated by dermal application of hapten, together suppress the generation of CTL. Thus, when tolerant mice possessing Ts-eff cells were concomitantly sensitized for CTL and CS (which causes the arisal of Ts-aux and TDTH effector cells), the development of CTL was suppressed. Furthermore, adoptive transfer of lymph node cells from dermally sensitized mice into tolerant mice also suppressed the CTL response. Use of lymph node cells from mice pretreated with cyclophosphamide before dermal sensitization and therefore lacking Ts-aux cells was not efficient in suppressing the CTL response. Thus, neither Ts-eff alone nor TDTH in conjunction with Ts-aux were capable of suppressing the development of CTL. In addition to supporting the view that the in vivo generation of CTL is suppressed when both Ts-eff and Ts-aux cells are present, the data indicate that suppressor cells operational for one T cell-mediated response (CS) are equally functional for a separate unrelated one (CTL).

No abstract

No abstract