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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Epithelial cells prime the immune response to an array of gut-derived commensals towards a tolerogenic phenotype through distinct actions of thymic stromal lymphopoietin and transforming growth factor-beta.
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Epithelial cells prime the immune response to an array of gut-derived commensals towards a tolerogenic phenotype through distinct actions of thymic stromal lymphopoietin and transforming growth factor-beta.

机译：上皮细胞通过胸腺基质淋巴细胞生成素和转化生长因子-β的独特作用，引发了对一系列肠道源性免疫应答的致耐受性表型。

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Humans and other mammals coexist with a diverse array of microbes colonizing the intestine, termed the microflora. The relationship is symbiotic, with the microbes benefiting from a stable environment and nutrient supply, and the host gaining competitive exclusion of pathogens and continuously maintenance of the gut immune homeostasis. Here we report novel crosstalk mechanisms between the human enterocyte cell line, Caco2, and underlying human monocyte-derived DC in a transwell model where Gram-positive (G+) commensals prevent Toll-like receptor-4 (TLR4)-dependent Escherichia coli-induced semimaturation in a TLR2-dependent fashion. These findings add to our understanding of the hypo-responsiveness of the gut epithelium towards the microflora. Gut DC posses a more tolerogenic phenotype than conventional DC. Here we show that Caco2 spent medium (SM) induces tolerogenic DC with lower expression of maturation markers, interleukin (IL)-12p70, and tumour necrosis factor-alpha when matured with G+ and Gram-negative (G-) commensals, while IL-10 production is enhanced in DC upon encountering G+ commensals and reduced upon encountering G- bacteria. The Caco2 SM-induced tolerogenic phenotype is also seen in DC priming of naive T cells with elevated levels of transforming growth factor-beta (TGF-beta) and markedly reduced levels of bacteria-induced interferon-gamma production. Caco2 cell production of IL-8, thymic stromal lymphopoietin (TSLP) and TGF-beta increases upon microbial stimulation in a strain dependent manner. TSLP and TGF-beta co-operate in inducing the tolerogenic DC phenotype but other mediators might be involved.
机译：人类和其他哺乳动物与定居在肠道中的多种微生物共存，称为微生物群。这种关系是共生的，微生物得益于稳定的环境和营养供应，宿主可以竞争性地排除病原体并持续维持肠道免疫稳态。在这里，我们报告了人类肠道细胞系，Caco2和潜在的人类单核细胞衍生的DC在Transwell模型中的新型串扰机制，在该模型中，革兰氏阳性（G +）共鸣可防止Toll样受体4（TLR4）依赖性大肠杆菌诱导依赖TLR2的方式进行半成熟。这些发现增加了我们对肠上皮对菌群反应不足的理解。肠道DC具有比常规DC更高的耐受性表型。在这里，我们显示，当与G +和革兰氏阴性（G-）推荐物一起成熟时，Caco2废培养基（SM）诱导具有较低表达的成熟标记物，白介素（IL）-12p70和肿瘤坏死因子-α的耐受性DC，而IL-遇到G +刺激时，DC的产量增加10，遇到G-细菌时，产量降低。 Caco2 SM诱导的致耐受性表型还出现在幼稚T细胞的DC引发中，该细胞的转化生长因子-β（TGF-β）水平升高，细菌诱导的干扰素-γ产生水平明显降低。 IL-8，胸腺基质淋巴细胞生成素（TSLP）和TGF-β的Caco2细胞产量在微生物刺激后以应变依赖性方式增加。 TSLP和TGF-beta在诱导耐受性DC表型方面合作，但可能涉及其他介体。

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