當(dāng)免疫細(xì)胞在人體充滿微生物的腸道中巡邏時(shí),，它們既能“容忍”無害的微生物,，又能攻擊和清除有潛在危險(xiǎn)的病原體,。在線發(fā)表在9月號(hào)《自然—免疫學(xué)》期刊上的一篇論文深化了我們對(duì)這一精致又動(dòng)態(tài)的過程的認(rèn)識(shí),。
以前的研究認(rèn)為,，一種名為T細(xì)胞的免疫細(xì)胞實(shí)施了對(duì)無害或共生的腸道微生物的免疫容忍,。Bali Pulendran和同事發(fā)現(xiàn)，雖然兩種名為巨噬細(xì)胞和樹突狀細(xì)胞的特定腸道“附屬”細(xì)胞在腸黏膜上互為鄰居,，但它們發(fā)揮的卻是截然相反的免疫功能,。巨噬細(xì)胞促進(jìn)調(diào)控T細(xì)胞的產(chǎn)生，而樹突狀細(xì)胞卻誘導(dǎo)潛在的致病性非調(diào)控T細(xì)胞的生產(chǎn),，這種非調(diào)控性T細(xì)胞能釋放促炎介質(zhì),。
全面認(rèn)識(shí)這種腸道附屬細(xì)胞群之間動(dòng)態(tài)合作的分子調(diào)控機(jī)制，還需要進(jìn)一步的研究（科學(xué)時(shí)報(bào)）。
原始出處:
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: [email protected]
