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Impairment of T Cell‐Mediated Immunity to Listeria monocytogenes in Pregnant Mice
Author(s) -
Sano Masatoshi,
Mitsuyama Masao,
Watanabe Yoshitsugu,
Nomoto Kikuo
Publication year - 1986
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.1986.tb00931.x
Subject(s) - spleen , listeria monocytogenes , immune system , immunology , biology , immunity , macrophage , listeria , antigen , immunization , cellular immunity , listeria infection , antibody , microbiology and biotechnology , in vitro , bacteria , biochemistry , genetics
In order to study pregnancy‐induced changes in cell‐mediated immunity to Listeria monocytogenes , acquired resistance and T cell functions in pregnant mice were compared with those in nonpregnant mice after immunization with viable listerial cells. Impaired generation of acquired resistance was evident in pregnant mice from the impaired elimination of bacteria and poor survival after secondary challenge. Delayed footpad reactivity to listerial antigen was also lower in the pregnant mice. When immune spleen cells were examined for their ability to produce macrophage activating factor in vitro , culture supernatants from pregnant‐mouse spleen cells with listerial antigen showed far less ability to render macrophages cytostatic for P815 mastocytoma cells. To elucidate further the impairment of listeria‐immune T cell generation in pregnant mice, a local transfer experiment was carried out. When a given number of immune spleen cells was transferred locally into the footpads of naive mice, both delayed footpad reaction and local protection were much lower in the pregnant mice. This local transferability of the reactions was abrogated after treatment of cells with anti‐Thy 1 antibody plus complement. These findings indicate that pregnancy impairs the generation of specific T cells capable of contributing to acquired resistance to L. monocytogenes . Possible mechanisms for this impairment and the relationship to macrophage functions are discussed.