I 型干扰素衰竭是一种宿主防御机制，可防止二次细菌感染。
Type I IFN exhaustion is a host defence protecting against secondary bacterial infections.
机构信息
Department of Emerging Pathogens and Vaccines, John Curtin School of Medical Research, Australian National University, Canberra, Australian Capital Territory, Australia.
出版信息
Scand J Immunol. 2013 Nov;78(5):395-400. doi: 10.1111/sji.12107.
Type I interferons (IFN-I) have been known for decades for their indispensable role in curtailing viral infections. It is, however, now also increasingly recognized that IFN-I is detrimental to the host in combating a number of bacterial infections. We have previously reported that viral infections induce partial lymphocyte activation, characterized by significant increases in the cell surface expression of CD69 and CD86, but not CD25. This systemic partial activation of lymphocytes, mediated by IFN-I, is rapid and is followed by a period of IFN-I unresponsiveness. Here we propose that IFN-I exhaustion that occurs soon after a primary viral infection may be a host response protecting it from secondary bacterial infections.
I 型干扰素 (IFN-I) 几十年来因其在抑制病毒感染方面的不可或缺的作用而为人所知。然而，现在也越来越多地认识到 IFN-I 在对抗一些细菌感染时对宿主有害。我们之前曾报道过，病毒感染会诱导部分淋巴细胞激活，其特征是细胞表面 CD69 和 CD86 的表达显著增加，但 CD25 没有增加。这种由 IFN-I 介导的淋巴细胞的全身性部分激活是迅速发生的，随后是一段 IFN-I 无反应期。在这里，我们提出，原发性病毒感染后很快发生的 IFN-I 耗竭可能是宿主对继发细菌感染的一种保护反应。
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