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Anti‐Parental Lymphocyte Reactions in Neonatal F l Hybrid Rats
Author(s) -
McCULLAGH P.
Publication year - 1977
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1977.tb00333.x
Subject(s) - fetus , lymphocyte , hybrid , strain (injury) , biology , immune system , immunology , antibody , in utero , phenotype , reactivity (psychology) , genetics , pregnancy , medicine , gene , pathology , anatomy , botany , alternative medicine
The subpopulation of parental‐strain lymphocytes responsible for the recognition of a particular F 1 hybrid strain as foreign has been shown to be subject to specific, reversible inactivation after its injection into neonatal rats of that F 1 hybrid strain. Neonates born to mothers that were syngeneic with the parental‐strain lymphocytes under test acquired the capacity to inactivate these lymphocytes at an earlier age than did the genotypically identical reciprocal F 1 hybrids. Neonates had little capacity to inactivate completely allogeneic lymphocytes. It is inferred from the difference in behavior between reciprocal F 1 hybrids that the augmented ability to inactivate anti‐F 1 hybrid maternal‐strain lymphocytes follows exposure to such cells in utero and to antibodies with anti‐F 1 hybrid activity in colostrum. Specific inactivation of those marauding maternal lymphocytes with anti‐fetal activity is envisaged as an important means of protection of the fetus from immunological attack by the mother. On the basis of the results presented in this and the preceding paper, it has been proposed that many of the sequelae of the transfer of immunocompetent parental‐strain cells to F 1 hybrid animals result not from graft anti‐host activity but from an F 1 hybrid anti‐parental lymphocyte response that has eluded normal regulatory mechanisms. These experiments also raise the possibility that regulation of auto‐immune responses may be achieved by the inactivation of lymphocytes with anti‐self reactivity by other lymphocytes that respond to the recognition structure required for such reactivity.