Key result
CCR5 deficiency in T. cruzi-infected mice dramatically inhibited T cell migration to the heart and increased susceptibility to infection.
Why the study?
Does CCR5 deficiency alter T cell migration to the heart and host susceptibility in mice infected with Trypanosoma cruzi?
Population
Mice infected with Trypanosoma cruzi (wild-type and CCR5-deficient models)
Comparison
CCR5 deficiency (genetic knockout) vs Wild-type mice with normal CCR5 expression
Design
Preclinical
Authors
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May implicate CCR5 in cardiac T-cell recruitment during Chagas myocarditis; leaves open whether blockade alters human outcomes.
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.
Machado et al. (2005) studied 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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