Solid organ transplantation, a major breakthrough in modern medicine, has saved countless patients with end-stage organ failure. However, immune rejection remains the primary obstacle to transplant success. As the central effector cells of adaptive immunity, T cells drive acute rejection by directly recognizing donor alloantigens (such as MHC molecules) or indirectly recognizing processed donor antigens presented by antigen-presenting cells. Recent studies have revealed the dual roles of distinct T cell subsets in rejection or tolerance: pro-inflammatory Th1, Th2, Th17, and CD8 + cytotoxic T cells(CTLs) exacerbate tissue damage by secreting cytokines such as IFN-γ and IL-17, whereas regulatory T cells(Tregs) promote graft tolerance by suppressing effector T cell activation and maintaining immune homeostasis. This article systematically reviews the molecular mechanisms of T cell-mediated rejection, functional heterogeneity among T cell subsets, and their differential impacts on various types of solid organ transplants.
Zhang et al. (Thu,) studied this question.