The adoptive cell transfer of cutaneous contact sensitivity (CS) in mice was employed to determine whether γδ T cells play a role in these responses. In vitro treatment of immunized CS effector T cells with monoclonal antibodies (mAb) to αβ T cell receptors (TCR) plus rabbit complement abolished the cell transfer of CS, as expected. However, surprisingly, so did similar treatment of CS effector cells with mAb to γδ TCR. Further experiments demonstrated that treatment with anti-γδ TCR or anti-αβ TCR mAb did not affect the early-acting, CS-initiating cell. However, mixing experiments showed that injection of the γδ T-remaining (αβ T-depleted) cells together with the αβ T-remaining (γδ T-depleted) cells fully reconstituted the transfer of 24-hour CS responses. It was concluded that in addition to CD3–– CS-initiating cells, and αβ TCR+ CS effector T cells, that a third population of γδ TCR+ T cells was required for elicitation of a 24-hour CS response. It was hypothesized that the γδ T cells acting in CS responses might recognize cell surface complexes of stress proteins and minor histocompatibility antigens which then mediate assistance of the antigen/MHC-class-II-specific αβ T cells to enable them to mediate 24-hour CS responses.

Keywords:
αβ T cells, γδ T cells, Delayed type hypersensitivity, Contact sensitivity allergy
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© 1992 S. Karger AG, Basel
1992
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