当免疫细胞在人体充满微生物的肠道中巡逻时，它们既能“容忍”无害的微生物，又能攻击和清除有潜在危险的病原体。在线发表在9月号《自然—免疫学》期刊上的一篇论文深化了我们对这一精致又动态的过程的认识。
以前的研究认为，一种名为T细胞的免疫细胞实施了对无害或共生的肠道微生物的免疫容忍。Bali Pulendran和同事发现，虽然两种名为巨噬细胞和树突状细胞的特定肠道“附属”细胞在肠黏膜上互为邻居，但它们发挥的却是截然相反的免疫功能。巨噬细胞促进调控T细胞的产生，而树突状细胞却诱导潜在的致病性非调控T细胞的生产，这种非调控性T细胞能释放促炎介质。
全面认识这种肠道附属细胞群之间动态合作的分子调控机制，还需要进一步的研究（科学时报）。
原始出处:
Nature Immunology 8, 1086 - 1094 (2007)
Published online: 16 September 2007 | doi:10.1038/ni1511
Lamina propria macrophages and dendritic cells differentially induce regulatory and interleukin 17–producing T cell responses
Timothy L Denning1, Yi-chong Wang1, Seema R Patel2, Ifor R Williams2 & Bali Pulendran1,2
The intestinal immune system must elicit robust immunity against harmful pathogens but must also restrain immune responses directed against commensal microbes and dietary antigens. The mechanisms that maintain this dichotomy are poorly understood. Here we describe a population of CD11b+F4/80+CD11c- macrophages in the lamina propria that expressed several anti-inflammatory molecules, including interleukin 10 (IL-10), but little or no proinflammatory cytokines, even after stimulation with Toll-like receptor ligands. These macrophages induced, by a mechanism dependent on IL-10, retinoic acid and exogenous transforming growth factor-, the differentiation of Foxp3+ regulatory T cells. In contrast, lamina propria CD11b+ dendritic cells elicited IL-17 production. This IL-17 production was suppressed by lamina propria macrophages, indicating that a dynamic interaction between these subsets may influence the balance between immune activation and tolerance.
Vaccine Research Center and Yerkes Regional Primate Research Center, Emory University, Atlanta, Georgia 30329, USA.
Department of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia 30322, USA.
Correspondence to: Bali Pulendran1,2 e-mail: bpulend@rmy.emory.edu
