Dendritic cell-mediated responses to secreted Cryptosporidium effectors promote parasite-specific CD8⁺ T cell responses.

ABSTRACT: Cryptosporidium causes debilitating diarrheal disease in patients with primary and acquired defects in T cell function. However, it has been a challenge to understand how this infection generates T cell responses and how they mediate parasite control. Here, Cryptosporidium was engineered to express a parasite effector protein (MEDLE-2) that contains the major histocompatibility complex-I restricted SIINFEKL epitope which is recognized by T cell receptor transgenic OT-I(OVA-TCR-I) clusters of differentiation (CD)8⁺ T cells. These modified parasites induced expansion of endogenous SIINFEKL-specific and OT-I CD8⁺ T cells that were a source of interferon-gamma (IFN-γ) that could restrict growth of Cryptosporidium. This T cell response was dependent on the translocation of

SUBMITTER: Haskins BE 

PROVIDER: S-EPMC11193387 | biostudies-literature | 2024 Jun

REPOSITORIES: biostudies-literature