Innate immunity for better or worse govern the allograft response.
Innate immunity for better or worse govern the allograft response.
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DOI：
10.1097/mot.0000000000000152
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发表时间：
2015-02
影响因子：
2.2
通讯作者：
Strom TB
中科院分区：
文献类型：
--
作者：
Otterbein LE;Fan Z;Koulmanda M;Thronley T;Strom TB
更新关于在移植期组织和细胞移植中不可避免地发生的有害形式的先天免疫的原因和后果的知识。此外，我们回顾了新发现的巨噬细胞群体的鉴定和特征，促进了植入和诱导耐受。同种异体移植物对适应性免疫细胞的应答是由先天免疫形成的。由于器官移植中的缺血再灌注损伤、细胞移植的延迟血运重建和缺氧所引起的先天免疫反应的激活，早期同种异体移植物的反应是独特强烈的。炎症是由细胞“碎片”和细胞因子共同产生的。另一方面，一个新发现的突出的，虽然脆弱，组织驻留，非侵入性和免疫调节巨噬细胞促进植入和耐受性。强调了细胞内“碎片”和炎症在引起有害排斥反应、引发移植周围炎症中的作用，以及一个突出的、高度免疫调节的、尽管脆弱的巨噬细胞群体的特征，这些巨噬细胞是组织驻留的，不循环。机会在于控制有害的移植期炎症的能力，以及促进高效组织驻留免疫调节巨噬细胞亚群寿命的能力。
To update knowledge concerning the cause and consequences of the detrimental forms of innate immunity that inevitably occurs in peri-transplant period tissue and cellular transplants. In addition we review information a newly discovered engraftment promoting and tolerance inducing macrophage population is identified and characterized. 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. On the other hand a newly discovered prominent, albeit fragile, tissue resident, non-invasive and immunoregulatory macrophage promotes engraftment and tolerance. The role of intracellular “debris” as well as inflammation in evoking detrimental rejection provoking peri-transplant 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. 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.