Type I interferons in bacterial infections: taming of myeloid cells and possible implications for autoimmunity.
Type I interferons in bacterial infections: taming of myeloid cells and possible implications for autoimmunity.
复制标题
DOI：
10.3389/fimmu.2014.00431
复制
发表时间：
2014
影响因子：
7.3
通讯作者：
Lenz LL
中科院分区：
文献类型：
--
作者：
Eshleman EM;Lenz LL
I型干扰素（IFN）首先被描述为它们保护宿主免受病毒感染的能力，并且在某些细菌感染的特定条件下也可能具有有益效果。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的感染，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。有证据表明，在动物和人类的细菌感染过程中都会发生这种有害影响，这就证明了选择性压力的存在。在这篇综述中，我们总结了证据表明，亲细菌的作用，I型干扰素，并讨论了可能的机制，已被提出来解释这种影响。出现的主题是，I型IFN抑制骨髓细胞免疫反应。这种抗炎作用的进化保守性，特别是在感染的情况下，表明它们可能对限制慢性炎症很重要。考虑到I型IFN在治疗某些自身免疫性疾病中的有效性，它们的产生也可以起到提高针对自身抗原的免疫应答激活的阈值的作用。
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.