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5 However, their role in the rejection of organ grafts has been difficult to highlight and is still a matter of debate. Their ability to distinguish allogeneic cells from self and their potent cytolytic effector function make NK cells relevant to allogeneic bone marrow transplantation. Consequently, in allotransplantation settings, interaction with fully mismatched allogeneic cells, lacking self MHC I molecules, leads to unopposed activating signals and NK-cell activation characterized by target cell killing and cytokine release. 3 Engagement of an excess of inhibitory receptors aborts the activating signaling cascades. 2, 3 Activating receptors recognize MHC class I-like molecules and other undefined ligands and trigger lysis and cytokine production. 2, 3 Inhibitory receptors encompass several families of cell surface molecules, such as Ly49 and CD94/NKG2 receptors in mouse, that recognize self-MHC class Ia molecules and transmit intracellular signals preventing NK-cell activation and target cell lysis. 1 Activation of NK cells results from the balance between the engagement of complex families of inhibitory and activatory receptors specific for major histocompatibility complex (MHC) I molecules and various others ligands. Natural killer (NK) cells are a major component of the innate immune system and are capable of killing target cells without prior immunization. Thus, NK cells act as early regulators of alloreactive T-cell priming in allotransplantation through their capacity to kill allogeneic DCs in draining lymph nodes. In normal mice, we further demonstrated that NK cells by quickly eliminating allogeneic DCs strongly inhibited alloreactive CD8 + T-cell responses. Moreover, we showed that Ly49D + CD127 − NK cells were recruited within DC draining lymph nodes and rapidly eliminated allogeneic H-2 d DCs through the perforin pathway. In CD8 + T cell–deficient C57BL/6 (H-2 b) recipients injected with allogeneic BALB/c (H-2 d) DCs, we demonstrated that NK cells expressing the H-2D d-specific Ly49D activating receptor were implicated in the regulation of alloreactive CD4 + T-cell responses.
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In a model of CD4 + T cell–mediated allogeneic skin graft rejection, we show that the absence of host NK-cell alloreactivity was characterized by enhanced expansion of alloreactive effector T lymphocytes, including Th2 cells, and massive eosinophilic infiltrates in the rejected tissues. Likewise, in solid organ transplantation, it has been recently shown that recipient NK cells may limit alloreactive T-cell responses through their capacity to prevent the persistence of graft-derived allogeneic dendritic cells (DCs). Natural killer (NK)–cell alloreactivity is exploited in bone marrow transplantation to improve clinical outcome.