Ferenbach David, Kluth David C, Hughes Jeremy
MRC Centre for Inflammation Research, University of Edinburgh, Queens Medical Research Centre, Edinburgh, United Kingdom.
Semin Nephrol. 2007 May;27(3):250-9. doi: 10.1016/j.semnephrol.2007.02.001.
Renal inflammation may result from a myriad of insults and often is characterized by the presence of infiltrating inflammatory leukocytes within the glomerulus or tubulointerstitium. Accumulating evidence indicates that infiltrating leukocytes are key players in the induction of renal injury. Although renal inflammation often is followed by the development of fibrosis with loss of renal function, it can resolve. Resolution may be spontaneous as in poststreptococcal glomerulonephritis or after the administration of effective treatment such as immunosuppressive agents. The mechanisms and cells underlying the resolution process and the exact temporal sequence remains uncertain at present but likely involves the removal of injurious leukocytes, the down-regulation of immune responses, and the alteration of the phenotype of infiltrating macrophages from proinflammatory to prorepair. In this review we examine the role of leukocytes in both renal inflammation and repair.
肾脏炎症可能由多种损伤因素引起,其特征通常是肾小球或肾小管间质中存在浸润性炎性白细胞。越来越多的证据表明,浸润的白细胞是导致肾损伤的关键因素。虽然肾脏炎症通常会继发纤维化并导致肾功能丧失,但也可能消退。消退可能是自发的,如在链球菌感染后肾小球肾炎中,或在给予有效治疗(如免疫抑制剂)后。目前,炎症消退过程的机制、细胞以及确切的时间顺序仍不确定,但可能涉及清除有害白细胞、下调免疫反应以及将浸润巨噬细胞的表型从促炎转变为促修复。在本综述中,我们探讨白细胞在肾脏炎症和修复中的作用。