Changes in the subsets of CD4 + T cells in Trypanosoma musculi infection: delay of immunological cure in young mice and the weak ability of aged mice to control the infection

After a 3 week course (approximately), during which there ismarked lymphoid hyperplasia, Trypanosoma musculi infectionsin young-adult mice are cured by an immune mechanism involvingantibodies of the IgG2a isotype. Both the lymphoid hyperplasiaand IgG2a antibody response are T-cell-dependent events andboth processes appear to be defective in aged mice. The purposeof the studies reported here was to elucidate the effects ofT.musculi infection on subsets of T cells for two reasons: (I)to gain insight into the probable roles of selected cytokines(IL-2, IL-4 and IFN-) in facilitating the production of curative,lgG2a antibodies, and (II) to examine the hypothesis that agingaffects the competence of CD4⁺ T cells to participate in immunologicalcontrol of infections. The major conclusions from these studiesare that: (I) T. musculi infection of mice induces rapid changein the CD4⁺ T cell population toward predominance of the activatedor memory (CD45RB^loCD44^hi) phenotype, cells which produce IFN-,II-3. IL-4 and IL-5, accompanied by profound Inhibition of IL-2production, and (II) in the old mice these changes are superimposedon the natural age-associated changes in the same direction(i.e. toward predominance of CD45RB^loCD44^hi T cells).Thus, inthe old animals, the combined changes of aging and infection,moving in the same direction, are devastating, resulting inthe aged animals being unable, or barely able, to control infection.