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[Ontogeny of T-cell recognition of self histocompatibility antigens: parenteral influences]
The existence of parental influences on the recognition of self histocompatibility was investigated. The results obtained showed that: 1) fetal liver and neonatal splenocytes and thymocytes from F1 mice differed in their capacity to regulate parental alloreactive T reactions against self histocompatibility antigens either of maternal or paternal origin. Fetal and neonatal F1 cells--until day 5--were able to suppress systemic and local GvH reactions induced in F1 hosts with maternal but not with paternal splenocytes; 2) this differential regulatory activity concerning parental GvH reactions against self histocompatibility antigens are correlated with the existence of a differential time lag in the appearance of thymic contrasuppressor activity on maternal anti-paternal and paternal anti-maternal GvH reactivity; 3) splenocytes from reciprocal F1 hybrids--from day 14 onwards--differed in their ability to stimulate F1 T cell proliferation in SMLC reactions; 4) foster nursing of F1 hybrids on mothers from the paternal strain was able to induce permanent alterations in the ability of their splenocytes to stimulate the proliferation of responder F1 T cells. The stimulatory ability of splenocytes from foster-nursed hybrids was indistinguishable from that observed in the reciprocal F1 combination nursed by their own mother, suggesting that lactation would be involved in the differences registered; 5) reciprocal F1 mice differed in their response to conventional antigens presented in the context of parental Ia antigens, lactation also being responsible for the induction of these differences. The different mechanisms involved in the alterations of the outcome of self recognition in the litter are discussed.
The existence of parental influences on the recognition of self histocompatibility was investigated. The results obtained showed that: 1) fetal liver and neonatal splenocytes and thymocytes from F1 mice differed in their capacity to regulate parental alloreactive T reactions against self histocompatibility antigens either of maternal or paternal origin. Fetal and neonatal F1 cells--until day 5--were able to suppress systemic and local GvH reactions induced in F1 hosts with maternal but not with paternal splenocytes; 2) this differential regulatory activity concerning parental GvH reactions against self histocompatibility antigens are correlated with the existence of a differential time lag in the appearance of thymic contrasuppressor activity on maternal anti-paternal and paternal anti-maternal GvH reactivity; 3) splenocytes from reciprocal F1 hybrids--from day 14 onwards--differed in their ability to stimulate F1 T cell proliferation in SMLC reactions; 4) foster nursing of F1 hybrids on mothers from the paternal strain was able to induce permanent alterations in the ability of their splenocytes to stimulate the proliferation of responder F1 T cells. The stimulatory ability of splenocytes from foster-nursed hybrids was indistinguishable from that observed in the reciprocal F1 combination nursed by their own mother, suggesting that lactation would be involved in the differences registered; 5) reciprocal F1 mice differed in their response to conventional antigens presented in the context of parental Ia antigens, lactation also being responsible for the induction of these differences. The different mechanisms involved in the alterations of the outcome of self recognition in the litter are discussed.