CCR5 deficiency in T. cruzi-infected mice dramatically inhibited T cell migration to the heart and increased susceptibility to infection.
Does CCR5 deficiency alter T cell migration to the heart and host susceptibility in mice infected with Trypanosoma cruzi?
CCR5 and its ligands are critical for mediating T cell influx into the heart during T. cruzi infection, highlighting a potential mechanistic target for managing Chagas disease myocarditis.
The pathogenesis of myocarditis during Trypanosoma cruzi infection is poorly understood. We investigated the role played by chemokine receptor 5 (CCR5) in the influx of T cells to the cardiac tissue of T. cruzi-infected mice. mRNA and protein for the CCR5 ligands CCL3, CCL4, and CCL5 were detected in the hearts of infected mice in association with CD4+ and CD8+ T cells. There was a high level of CCR5 expression on CD8+ T cells in the hearts of infected mice. Moreover, CCR5 expression on CD8+ T cells was positively modulated by T. cruzi infection. CCR5-deficient mice infected with T. cruzi experienced a dramatically inhibited migration of T cells to the heart and were also more susceptible to infection. These results suggest that CCR5 and its ligands play a central role in the control of T cell influx in T. cruzi-infected mice. Knowledge of the mechanisms that trigger and control the migration of cells to the heart in patients with Chagas disease may help in the design of drugs that prevent myocarditis and protect against the development of severe disease.
Machado et al. (Sat,) conducted a other in Trypanosoma cruzi infection (myocarditis). CCR5 deficiency vs. CCR5-sufficient mice (implied) was evaluated on Migration of T cells to the heart and susceptibility to infection. CCR5 deficiency in T. cruzi-infected mice dramatically inhibited T cell migration to the heart and increased susceptibility to infection.
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