Innate immunity for better or worse govern the allograft response

Purpose of review To update knowledge concerning the cause and consequences of the detrimental forms of innate immunity that inevitably occurs in peritransplant period tissue and cellular transplants. In addition, we review the information that a newly discovered, engraftment-promoting, and tolerance-inducing macrophage population is identified and characterized. Recent findings The allograft response mounted by adaptive immune cells is shaped by innate immunity. The early allograft response is uniquely intense as a result of activation of the innate immune response created by ischemia reperfusion injury in organ transplants, delayed revascularization of cell transplants, and hypoxia. Inflammation is created by both cellular 'debris' and cytokines. However, a newly discovered prominent, albeit fragile, tissue-resident, noninvasive, and immunoregulatory macrophage promotes engraftment and tolerance. The role of intracellular 'debris' as well as inflammation in evoking detrimental rejection-provoking peritransplant inflammation is emphasized as well as characterization of a prominent and highly immunoregulatory albeit fragile macrophage population that is tissue-resident and does not circulate is characterized. Summary Opportunity lies in the ability to rein in detrimental peri-transplant inflammation and in the ability to promote the longevity of a subpopulation of highly potent tissue-resident immunoregulatory macrophages.