Major histocompatibility complex class I and II deficient knock-out mice are resistant to primary but susceptible to secondary Eimeria papillata infections

Two distinct mechanisms seem to function in reducing oocyst output during Eimeria papillata infections in mice. For naive mice, immunity was afforded by a T-cell-independent gamma-interferon (IFN-gamma) response mediated by natural killer (NK) cells. On reinfection, resistance was associated with T-cells and, to a lesser extent, perforin. To determine if antigen presentation with major histocompatibility complex (MHC) molecules was required to control oocyst production by NK cells during primary infection or by T-cells during secondary infection, mutant mice that lacked H2-IA beta b (A beta b(-/-)) or beta 2-microglobulin (beta 2m(-/-)) were used. Since MHC molecules are required for the maturation of alpha beta T-cells, A beta b(-/-) and beta 2m(-/-) mutant mice are also deficient in functional alpha beta(+)CD4(+) or alpha beta(+)CD8(+) T-cells, respectively. As compared with wild-type control mice, oocyst output by mutant mice was not significantly affected during primary infection, suggesting that the ability of NK cells to control parasite replication is not dependent on the expression of MHC molecules. On reinfection, differences were observed for mutant mice as compared with controls. A beta b(-/-) mice were found to be more susceptible than beta 2m(-/-) mice, suggesting that the alpha beta(+)CD4(+) T-cell subset plays a greater role in resistance to reinfection than does the alpha beta(+)CD8(+) T-cell subset. The mechanism of resistance depends on the immune status of the host and requires the coordinated interaction of both alpha beta(+) T-cell subsets for optimal parasite control during subsequent infections.