62 research outputs found

    Phenotypic expression of genetically controlled host resistance to Listeria monocytogenes.

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    Several inbred mouse strains, all of them derived from the C57BL background, have genetically determined increased resistance to infection with Listeria monocytogenes, whereas a variety of other strains are relatively sensitive to this infection. Comparison of the host response to L. monocytogenes in the sensitive A strain and the resistant C57BL/6 (B6) strain revealed that the B6 mice were superior to A mice both in the T-cell-independent and in the T-cell-dependent phase of the response. Although animals of both strains had equal ability to clear their circulation of intravenously administered Listeria and to take up comparable amounts of bacteria in their livers and spleens, already 24 to 48 h after infection the genetic advantage of B6 strain mice to suppress bacterial proliferation was apparent. Both the primary (early and late) and the secondary responses as well as the ability to inactivate the bacterial load after adoptive protection by syngeneic immune lymphocytes were more efficient in the B6 animals, suggesting that the common effector macrophage arm of the antilisterial resistance rather than the lymphocyte arm (mediating the T-cell-dependent phase of response) is genetically controlled

    The effect of dietary amino acids on immune reactivity.

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    The plaque-forming cell response and serum antibody titres to sheep red blood cells (SRBC) were enhanced in mice fed diets moderately deficient in the amino acids phenylalanine-tyrosine. These diets sustained normal growth during a 4 week study period. More severe limitation of phenylalanine-tyrosine or multiple essential amino acid restriction gave rise to a slight increas in the delayed hypersensitivity reaction to SRBC. These latter diets usually limit growth; nevertheless the humoral immune response to SRBC was not significantly depressed except in the mice fed a diet (diet 7) with severe restriction of seven essential amino acids. These results suggest that dietary restriction may suppress the production or function of an inhibitory cell, such as a suppressor T cell, whilst not affecting the effector cell to the same degree
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