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Distinct populations of donor and recipient macrophages coexist within the transplanted heart. Donor CCR2⁺ macrophages are key mediators of allograft rejection, and deletion of MYD88 signaling in donor macrophages is sufficient to suppress rejection and extend allograft survival. This highlights the therapeutic potential of donor heart-based interventions.
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Kopecky et al. (2022) studied this question.
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