Authors
Yukai Tang, Joel S Freibaum, Gregory S Cohen, Riley P Leathem, Scott M Krummey
Published in
Transplant immunology. Pages 102460. Sep 24, 2026. Epub Sep 24, 2026.
Abstract
Upon recognition of alloantigen, T cells rely on an array of costimulatory and coinhibitory receptors to shape their activation and function. The surface receptor CD43 has been reported to provide myriad functions on T cell related to adhesion, trafficking, and intracellular signaling. We investigated the role of CD43 on CD8+ T cells in vitro and in a fully allogeneic model of acute allograft rejection. Following polyclonal activation, CD43 did not impact the initial proliferation of CD8+ T cells, although CD43 deficient CD8+ T cells had mildly enhanced expression of IL-2Rα and PD-1 relative to CD43 wild-type CD8+ T cells (***p = 0.0008 and **p = 0.006, respectively). Following 7-9 days of in vitro culture, CD43 deficient CD8+ T cells had a stronger effector phenotype, displaying greater expression of Granzyme B, CD69, IL-2Rα, and PD-1. Following fully allogeneic skin grafting, alloantigen-specific CD43 deficient CD8+ T cells accumulated at greater numbers in the secondary lymphoid tissue and the allograft relative to CD43 wild-type CD8+ T cells (draining lymph nodes ***p = 0.007, spleen *p = 0.03). Hierarchical clustering and manual gating of revealed that CD43 deficient had an elevated frequency of effector populations with a CD62Llo, KLRG-1+, and CD49dhi phenotype, and that CD43 KO CD49dhi cells preferentially infiltrated the allograft tissue (***p = 0.0001). Together, these data provide evidence that CD43 acts as a checkpoint of alloantigen-specific CD8+ T cell differentiation after transplantation.
PMID:
42785691
Bibliographic data and abstract were imported from PubMed on 25 Sep 2026.
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