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Chemokine receptor type 3 (CXCR3) plays an important role in CD8 +  T cells migration during intracellular infections, such as  Trypanosoma cruzi . In addition to chemotaxis, CXCR3 receptor has been described as important to the interaction between antigen-presenting cells and effector cells. We hypothesized that CXCR3 is fundamental to  T .  cruzi -specific CD8 +  T cell activation, migration and effector function. Anti-CXCR3 neutralizing antibody administration to acutely  T .  cruzi -infected mice decreased the number of specific CD8 +  T cells in the spleen, and those cells had impaired in activation and cytokine production but unaltered proliferative response. In addition, anti-CXCR3-treated mice showed decreased frequency of CD8 +  T cells in the heart and numbers of plasmacytoid dendritic cells in spleen and lymph node. As CD8 +  T cells interacted with plasmacytoid dendritic cells during infection by  T .  cruzi , we suggest that anti-CXCR3 treatment lowers the quantity of plasmacytoid dendritic cells, which may contribute to impair the prime of CD8 +  T cells. Understanding which molecules and mechanisms guide CD8 +  T cell activation and migration might be a key to vaccine development against Chagas disease as those cells play an important role in  T .  cruzi  infection control.

CXCR3 chemokine receptor contributes to specific CD8+ T cell activation by pDC during infection with intracellular pathogens