Tatano Yutaka, Shimizu Toshiaki, Tomioka Haruaki
Department of Microbiology and Immunology, Shimane University School of Medicine, Izumo, Shimane 693-8501, Japan.
Sci Rep. 2014 Feb 20;4:4146. doi: 10.1038/srep04146.
Mycobacterial infection induces suppressor macrophages (MΦs), causing disease exacerbation. There are two major MΦ subsets (M1 and M2 MΦs) that are phenotypically and functionally different. Here, we examined which of the MΦ subsets the mycobacterial infection-induced suppressor MΦs (MIS-MΦs) belong to. MIS-MΦs down-regulated T cell production of Th1 and Th2 cytokines but markedly increased production of interleukin (IL)-17A and IL-22 through up-regulation of Th17 cell expansion. In this phenomenon, a novel MΦ population, which is functionally distinguishable from M1 and M2 MΦ subsets and possesses unique phenotypes (IL-12(+), IL-1β(high), IL-6(+), tumor necrosis factor (TNF)-α(+), nitric oxide synthase (NOS) 2(+), CCR7(high), IL-10(high), arginase (Arg)-1(-), mannose receptor (MR)(low), Ym1(high), Fizz(low), and CD163(high)), played central roles through the action of IL-6 and transforming growth factor (TGF)-β but not IL-21 and IL-23. This new type of MΦ population was induced in infected mice and actively supported the in vivo expansion of Th17 cells.
分枝杆菌感染会诱导抑制性巨噬细胞（MΦs）产生，从而导致疾病加重。存在两种主要的MΦ亚群（M1和M2 MΦs），它们在表型和功能上有所不同。在此，我们研究了分枝杆菌感染诱导的抑制性MΦs（MIS-MΦs）属于哪种MΦ亚群。MIS-MΦs下调了Th1和Th2细胞因子的T细胞产生，但通过上调Th17细胞扩增显著增加了白细胞介素（IL）-17A和IL-22的产生。在这一现象中，一种新型的MΦ群体发挥了核心作用，该群体在功能上可与M1和M2 MΦ亚群区分开来，并具有独特的表型（IL-12(+)、IL-1β(高)、IL-6(+)、肿瘤坏死因子（TNF）-α(+)、一氧化氮合酶（NOS）2(+)、CCR7(高)、IL-10(高)、精氨酸酶（Arg）-1(-)、甘露糖受体（MR）(低)、Ym1(高)、Fizz(低)和CD163(高)），其作用是通过IL-6和转化生长因子（TGF）-β而非IL-21和IL-23介导的。这种新型的MΦ群体在感染小鼠中被诱导产生，并积极支持Th17细胞在体内的扩增。
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