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Alloimmune response modulation refers to approaches aimed at altering the immune system’s reaction to alloantigens—antigens present on tissues or cells from genetically non-identical individuals of the same species[1][2][3][5]. In transplantation, the alloimmune response is central to graft rejection, involving host T lymphocytes recognizing foreign MHC (major histocompatibility complex) molecules on donor tissue, along with the generation of alloantibodies to donor antigens[1][2][3]. Modulating this response is vital for successful organ and cell transplantation and for the management of graft-versus-host disease. Approaches include immunosuppressive drugs (e.g., corticosteroids, calcineurin inhibitors, biologic DMARDs)[7], cytokine antagonists, costimulatory blockade (targeting CD28/B7 pathways), and novel cellular therapies aiming to promote immune tolerance[5][7]. Alloimmune response modulation is a therapeutic strategy, not a discrete drug target, receptor, or protein. Immunomodulators such as corticosteroids, calcineurin inhibitors, biologics, and cell therapies are used to modulate alloimmune responses in clinical transplantation, but their targets include molecules like T cell receptors, costimulatory molecules (CD28, CD80/86), cytokine receptors, and others[7][2]. Common mechanisms include dampening T cell activation, inhibiting cytokine production, suppressing memory and effector T cell responses, and interfering with antigen presentation[1][2][7]. In summary: “Alloimmune response modulation” is a therapeutic strategy or process, not an individual receptor, enzyme, or protein target. It does not meet the definition of a canonical molecular target.
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