Doherty Terence M, Arditi Moshe
Atherosclerosis Research Center, Division of Cardiology, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA.
J Clin Invest. 2004 Dec;114(12):1699-703. doi: 10.1172/JCI23867.
Innate immunity critically depends on signaling by Toll-like receptors (TLRs) that rely heavily on an intracellular adapter protein called myeloid differentiation factor 88 (MyD88). Adaptive immune defenses are generally thought to be orchestrated by innate immune responses and so should require intact TLR-MyD88 signaling pathways. But a surprising new study in MyD88-null mice infected with Mycobacterium tuberculosis challenges this view and instead suggests that MyD88 may not be absolutely required for a normal adaptive immune response.
固有免疫严重依赖于Toll样受体（TLR）信号传导，而这在很大程度上依赖于一种名为髓样分化因子88（MyD88）的细胞内衔接蛋白。适应性免疫防御通常被认为是由固有免疫反应精心安排的，因此应该需要完整的TLR-MyD88信号通路。但是，一项针对感染结核分枝杆菌的MyD88基因敲除小鼠的惊人新研究对这一观点提出了挑战，反而表明正常的适应性免疫反应可能并非绝对需要MyD88。
