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C3H/HeJ mice received B10.BR skin grafts following portal or lateral tail vein infusion of irradiated B10.BR spleen cells. Thereafter mice were injected with anti‐αβ or anti‐γδ T‐cell receptor (TCR) monoclonal antibody (mAb). Anti‐γδ TCR mAb abolished the increased graft survival afforded by portal venous (p.v.) immunization, and reversed the bias towards expression of mRNA for type‐2 cytokines [interleukin‐4 (IL‐4), IL‐10] seen in lymphoid tissue of p.v.‐immunized mice. When γδ TCR+ and αβ TCR+ cells were isolated from the intestinal epithelial compartment (IEL), liver or Peyer's Patch (PP) of p.v.‐immunized mice, the γδ TCR+ cells were found to be enriched in cells producing type‐2 cytokines on rechallenge with irradiated B10.BR cells in vitro. γδ TCR+ cells from p.v.‐immunized mice were further expanded in vitro with anti‐CD3 and cytokines (combined IL‐2 and IL‐4). Following expansion these cells were capable of adoptively transferring increased B10.BR skin graft survival to naive mice, and continued to show a bias in type‐2 cytokine synthesis after allostimulation in vitro. When γδ TCR chain expression was assessed in cells taken from p.v.‐immunized mice, or in cells expanded in culture, our data suggest that p.v. immunization leads to oligoclonal, not polyclonal, expansion of those γδ TCR+ cells involved in inhibition of graft rejection.

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