CD4⁺ effector and memory cell populations protect against Cryptosporidium parvum infection.

Cryptosporidium parvum is a protozoan parasite that infects the epithelial cells of the small intestine causing diarrheal illness in humans. While T cells are known to be important in resistance and recovery from infection, little has been characterized as to the phenotypic expression of surface effector and memory markers after infection. We used an acute model of infection (C57BL/6 interleukin-12p40), which develops long-standing resistance to re-infection, to characterize expression of different effector and memory cells. Using flow cytometry, we found that heterogeneous populations were generated after infection, consisting of both CD62L(high) central memory T cells (T(CM)) and CD62L(low) effector memory T cells (T(EM)) that were competent to produce the Th type 1 effector cytokine, IFN-γ. Both CD4⁺ and CD8⁺ T(CM) and T(EM) populations persisted in the absence of infection (up to 60 days post-infection). Additionally, transfer of either CD62L(low)CD4⁺ T(EM) or CD62L(high)CD4⁺ T(CM) into naive recipients resulted in a protective response. Taken together, these studies show that distinct subsets of effector and memory CD4⁺ T cells develop after infection with C. parvum, and mediate protective immunity to re-challenge.