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外文期刊>european journal of immunology
>Non‐H‐2‐associated genetic regulation of cytotoxic responses to hapten‐modified syngeneic cells Effect on the magnitude of secondary response and helper T cell generation afterin vivopriming
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Non‐H‐2‐associated genetic regulation of cytotoxic responses to hapten‐modified syngeneic cells Effect on the magnitude of secondary response and helper T cell generation afterin vivopriming
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机译:Non‐H‐2‐associated genetic regulation of cytotoxic responses to hapten‐modified syngeneic cells Effect on the magnitude of secondary response and helper T cell generation afterin vivopriming
AbstractThe present study investigates the role of non‐H‐2 genes in controlling generation of the H‐2‐restricted, T cell‐mediated cytotoxic response against trinitrophenyl (TNP)‐modified syngeneic cells (TNP‐self). Spleen cells from C3H/He (H‐2k) or B10.BR (H‐2k) normal mice or from mice primed to TNPin vivoby skin painting with trinitro‐chlorobenzene were used (a) forin vitrosensitization to TNP‐self and (b) as a source of radioresistant helper cells for augmenting the TNP‐self cytotoxic T lymphocyte (CTL) response generated by normal syngeneic spleen cells. Although spleen cells from unprimed mice from these two strains exhibited a comparable CTL response in a primary culture, a strong difference was observed in a secondary CTL response afterin vivopriming. CTL activities generated in the secondary culture were much stronger in C3H/He than in B10.BR strains. This difference in the magnitude of secondary CTL responses was paralleled by generation of strong and weak helper cell activity in C3H/He and B10.BR, respectively. No detectable difference was observed between the two H‐2kstrains in the lysability of target cells and ability of stimulating cells to activate the primed unirradiated cells and radioresistant helper cells. This genetic difference detected in the H‐2khaplotype was also demonstrated in the H‐2bhaplotype, by using C3H.SW and C57BL/10 mice which bear non‐H‐2 background genes corresponding to C3H/He and B10.BR mice, respectively. These results indicate the existence of a control mechanism influenced by non‐H‐2 genes, in addition to th
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