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The interaction between donor T-cells (lymphocytes from a transplant donor) and antigen-presenting cells (APCs) (including dendritic cells, macrophages, and B cells from either donor or host origin) is central to immune processes such as transplant rejection, graft-versus-host disease, infection, and tumor immunity. In the context of transplantation, donor T-cells recognize and respond to antigens presented by host or donor APCs via three main pathways: direct (T-cell recognition of intact allo-MHC on donor APCs), indirect (T-cell recognition of donor-derived peptides presented by host APCs), and semidirect (recipient APCs presenting acquired donor MHC to T-cells)[1][5][4]. This interaction is mediated through antigen presentation by major histocompatibility complex (MHC) molecules, costimulatory signals (e.g., CD28, CD40L), and various cytokines and adhesion molecules[4][5][6]. While essential for immune defense and establishing tolerance, dysregulation of this interaction can provoke pathological immune responses, such as allograft rejection or chronic inflammation.
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