The decline of immunological resistance of aging mice to Trypanosoma musculi.
Aged mice of several strains studied developed much more severe infections of Trypanosoma musculi (mouse-specific parasite) than did young adults. Reduced resistance of the aged mice, assessed from the resistance conferred on irradiated recipients by transfer of normal and infected donor spleen cells, resulted from a much slower development of immunity to the parasite, reflecting depleted immune competence, and from the expression in aged mice of an altered internal milieu unfavorable for normal function of lymphoid cells. An analysis of antibody-dependent cytotoxic reactions against T. musculi revealed no differences; therefore, intrinsic changes in antibody-dependent cytotoxic effector cells are not responsible for the decline in resistance to trypanosomes. The possibility that quantitative or qualitative changes in humoral antibody production might account for defective resistance of aged mice was minimized by demonstrating that antibodies play a minor role in the recovery from infection with T. musculi. Evidence of a significant role (possibly indirect) of macrophages in resistance to T. musculi was obtained. Altogether, our data raise the possibility that the decline in natural killer activity that is susceptible to amplification by macrophage-derived interferon may account for the defective resistance of aged mice to trypanosomes.
D000375:Aging; D000818:Animals; D000906:Antibodies; D000920:Antibody-Dependent Cell Cytotoxicity; D007109:Immunity; D007116:Immunization, Passive; D051379:Mice; D008815:Mice, Inbred Strains; D013154:Spleen / Q000276:immunology; D014352:Trypanosomiasis / Q000276:immunology*
D000906:Antibodies