Eshleman Emily M, Lenz Laurel L
Department of Immunology and Microbiology, University of Colorado School of Medicine , Aurora, CO , USA.
Department of Immunology and Microbiology, University of Colorado School of Medicine , Aurora, CO , USA ; Department of Biomedical Research, National Jewish Health , Denver, CO , USA.
Front Immunol. 2014 Sep 11;5:431. doi: 10.3389/fimmu.2014.00431. eCollection 2014.
Type I interferons (IFNs) were first described for their ability to protect the host from viral infections and may also have beneficial effects under specific conditions within some bacterial infections. Yet, these pleiotropic cytokines are now known to exacerbate infections by numerous life-threatening bacteria, including the intracellular pathogens Listeria monocytogenes and Mycobacterium tuberculosis. The evidence that such detrimental effects occur during bacterial infections in both animals and humans argues for selective pressure. In this review, we summarize the evidence demonstrating a pro-bacterial role for type I IFNs and discuss possible mechanisms that have been proposed to explain such effects. The theme emerges that type I IFNs act to suppress myeloid cell immune responses. The evolutionary conservation of such anti-inflammatory effects, particularly in the context of infections, suggests they may be important for limiting chronic inflammation. Given the effectiveness of type I IFNs in treatment of certain autoimmune diseases, their production may also act to raise the threshold for activation of immune responses to self-antigens.
I型干扰素（IFNs）最初因其保护宿主免受病毒感染的能力而被描述，并且在某些细菌感染的特定条件下可能也具有有益作用。然而，现在已知这些多效性细胞因子会加剧许多危及生命的细菌感染，包括细胞内病原体单核细胞增生李斯特菌和结核分枝杆菌。在动物和人类的细菌感染过程中出现这种有害作用的证据表明存在选择性压力。在这篇综述中，我们总结了证明I型干扰素具有促细菌作用的证据，并讨论了为解释此类作用而提出的可能机制。出现的主题是I型干扰素起到抑制髓样细胞免疫反应的作用。这种抗炎作用在进化上的保守性，特别是在感染的背景下，表明它们对于限制慢性炎症可能很重要。鉴于I型干扰素在治疗某些自身免疫性疾病方面的有效性，它们的产生也可能起到提高对自身抗原免疫反应激活阈值的作用。
