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CD101 as an indicator molecule for pathological changes at the interface of host-microbiota interactions
International Journal of Medical Microbiology ( IF 4.1 ) Pub Date : 2021-03-20 , DOI: 10.1016/j.ijmm.2021.151497
Marius Wrage 1 , Johanna Kaltwasser 1 , Sonja Menge 1 , Jochen Mattner 2
Affiliation  

Intestinal microbiota signal to local and distant tissues in the body. Thus, they also regulate biochemical, metabolic and immunological processes in the gut and in the pancreas. Vice versa, eating habits or the immune system of the host shape the intraluminal microbiota. Disruptions of these versatile host-microbiota interactions underlie the pathogenesis of complex immune-mediated disorders such as inflammatory bowel disease (IBD) or type 1 diabetes (T1D). Consequently, dysbiosis and increased intestinal permeability associated with both disorders change the biology of underlying tissues, as evidenced, for example, by an altered expression of surface markers such as CD101 on immune cells located at these dynamic host-microbiota interfaces.

CD101, a heavily glycosylated member of the immunoglobulin superfamiliy, is predominantly detected on myeloid cells, intraepithelial lymphocytes (IELs) and regulatory T cells (Tregs) in the gut. The expression of CD101 on both myeloid cells and T lymphocytes protects from experimental enterocolitis and T1D. The improved outcome of both diseases is associated with an anti-inflammatory cytokine profile and a reduced expansion of T cells. However, distinct bacteria suppress the expression of CD101 on myeloid cells, similar as does inflammation on T cells. Thus, the reduced CD101 expression in T1D and IBD patients might be a consequence of an altered composition of the intestinal microbiota, enhanced bacterial translocation and a subsequent primining of local and systemic inflammatory immune responses.



中文翻译:

CD101作为宿主-微生物相互作用界面病理变化的指示分子

肠道微生物群向身体局部和远处组织发出信号。因此,它们还调节肠道和胰腺中的生化、代谢和免疫过程。反之亦然,饮食习惯或宿主的免疫系统塑造了腔内微生物群。这些多功能宿主-微生物群相互作用的破坏是复杂免疫介导疾病的发病机制,例如炎症性肠病 (IBD) 或 1 型糖尿病 (T1D)。因此,与这两种疾病相关的菌群失调和肠道通透性增加改变了底层组织的生物学特性,例如,位于这些动态宿主-微生物群界面的免疫细胞上表面标志物(如 CD101)的表达改变就证明了这一点。

CD101 是免疫球蛋白超家族中高度糖基化的成员,主要在肠道中的骨髓细胞、上皮内淋巴细胞 (IEL) 和调节性 T 细胞 (Treg) 上检测到。CD101 在骨髓细胞和 T 淋巴细胞上的表达可以防止实验性小肠结肠炎和 T1D。这两种疾病的改善结果与抗炎细胞因子谱和 T 细胞扩增减少有关。然而,不同的细菌会抑制骨髓细胞上 CD101 的表达,这与 T 细胞上的炎症类似。因此,T1D 和 IBD 患者 CD101 表达降低可能是肠道微生物群组成改变、细菌易位增强以及随后引发局部和全身炎症免疫反应的结果。

更新日期:2021-03-25
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