Center for Neurologic Diseases, Brigham and Women's Hospital, Boston, MA, USA.
J Immunol. 2010 Feb 15;184(4):1710-20. doi: 10.4049/jimmunol.0902796. Epub 2010 Jan 18.
IL-23 plays an important role in autoimmune tissue inflammation and induces the generation of not fully characterized effector cells that mediate protection against pathogens. In this paper, we established the essential role of IL-23R in the host response against intracellular pathogens. IL-23 was critical for the expansion or maintenance of gammadelta and double negative (DN) alphabeta T cells. These cells were rapidly recruited to the site of infection and produced large amounts of IL-17, IFN-gamma, and TNF-alpha. Notably, DN T cells transferred into L. monocytogenes-infected RAG2(-/-) mice prevented bacterial growth, confirming their protective role against intracellular pathogens. Our results show that IL-23 regulates the function of IL-17-producing gammadelta and DN T cells, two essential components of the early protective immune response directed against intracellular pathogens.
白细胞介素-23(IL-23)在自身免疫性组织炎症中发挥重要作用,并诱导产生不完全特征的效应细胞,介导对病原体的保护。在本文中,我们确立了 IL-23R 在宿主对细胞内病原体的反应中的重要作用。IL-23 对于 gammadelta 和双阴性(DN)alphabeta T 细胞的扩增或维持至关重要。这些细胞迅速募集到感染部位,并产生大量的白细胞介素-17(IL-17)、干扰素-γ(IFN-γ)和肿瘤坏死因子-α(TNF-α)。值得注意的是,转移到李斯特菌感染的 RAG2(-/-) 小鼠中的 DN T 细胞可防止细菌生长,证实了它们对细胞内病原体的保护作用。我们的结果表明,IL-23 调节产生白细胞介素-17 的 gammadelta 和 DN T 细胞的功能,这是针对细胞内病原体的早期保护性免疫反应的两个重要组成部分。