Key result
CCR5-deficient mice rapidly reject cardiac allografts within 14 days compared to wild-type recipients.
Why the study?
Mechanisms of class I MHC antibody-mediated cardiac allograft injury remain unclear and require investigation in relevant murine models.
Population
Murine recipients including wild-type C57BL/6 and various knockout strains receiving heart allografts
Comparison
B6.K(d) heart allografts in CCR5(-/-) and knockout recipients versus wild-type C57BL/6 recipients
Design
Preclinical experimental study using transgenic and knockout murine models
Follow-up
Up to 60 days
Authors
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CCR5 deficiency accelerates class I MHC-disparate cardiac allograft rejection in mice; leaves open relevance to human transplant outcomes.
Continual production of antidonor class I MHC antibody can mediate cardiac allograft rejection, and donor-reactive CD8 T cells synergize with the antibody to contribute to rejection.
Hattori et al. (2012) studied Cardiac allograft rejection. CCR5(-/-) knockout vs. Wild-type C57BL/6 recipients was evaluated on Allograft survival. CCR5(-/-) mice rejected single class I MHC-disparate cardiac allografts within 14 days, whereas allografts survived longer than 60 days in wild-type recipients.
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