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1
MAIT Cells in Health and Disease.MAIT 细胞在健康与疾病中的作用
Methods Mol Biol. 2020;2098:3-21. doi: 10.1007/978-1-0716-0207-2_1.
2
Interleukin-17 Inhibition in Spondyloarthritis Is Associated With Subclinical Gut Microbiome Perturbations and a Distinctive Interleukin-25-Driven Intestinal Inflammation.白细胞介素-17 抑制在脊柱关节炎中与亚临床肠道微生物组紊乱和独特的白细胞介素-25 驱动的肠道炎症有关。
Arthritis Rheumatol. 2020 Apr;72(4):645-657. doi: 10.1002/art.41169. Epub 2020 Mar 12.
3
Keratinocyte-intrinsic MHCII expression controls microbiota-induced Th1 cell responses.角质形成细胞固有 MHCII 表达控制微生物群诱导的 Th1 细胞应答。
Proc Natl Acad Sci U S A. 2019 Nov 19;116(47):23643-23652. doi: 10.1073/pnas.1912432116. Epub 2019 Oct 31.
4
Shotgun metagenomics reveals an enrichment of potentially cross-reactive bacterial epitopes in ankylosing spondylitis patients, as well as the effects of TNFi therapy upon microbiome composition. shotgun 宏基因组学揭示了强直性脊柱炎患者中潜在交叉反应性细菌表位的富集，以及 TNFi 治疗对微生物组组成的影响。
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Immune cells for microbiota surveillance.用于微生物群监测的免疫细胞。
Science. 2019 Oct 25;366(6464):419-420. doi: 10.1126/science.aaz4014.
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MAIT cells are imprinted by the microbiota in early life and promote tissue repair.MAIT 细胞在生命早期受到微生物群的印记，并促进组织修复。
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CD109 Restrains Activation of Cutaneous IL-17-Producing γδ T Cells by Commensal Microbiota.CD109 抑制共生菌群激活皮肤产生 IL-17 的 γδ T 细胞。
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8
STAT3 but not STAT4 is critical for γδT17 cell responses and skin inflammation.STAT3 而非 STAT4 对于 γδT17 细胞应答和皮肤炎症至关重要。
EMBO Rep. 2019 Nov 5;20(11):e48647. doi: 10.15252/embr.201948647. Epub 2019 Sep 24.
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Significance of IL-17A-producing CD8CD103 skin resident memory T cells in psoriasis lesion and their possible relationship to clinical course.IL-17A 产生的 CD8+CD103+皮肤归巢记忆 T 细胞在银屑病皮损中的意义及其与临床病程的可能关系。
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10
c-Kit-positive ILC2s exhibit an ILC3-like signature that may contribute to IL-17-mediated pathologies.c-Kit 阳性 ILC2s 表现出 ILC3 样特征，这可能有助于 IL-17 介导的病理过程。
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脊柱关节炎中的屏障淋巴细胞。

Barrier lymphocytes in spondyloarthritis.

机构信息

Division of Rheumatology, University of Colorado School of Medicine, Aurora, Colorado, USA.

出版信息

Curr Opin Rheumatol. 2020 Jul;32(4):343-348. doi: 10.1097/BOR.0000000000000716.

DOI:10.1097/BOR.0000000000000716
PMID:32412993
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7871527/
Abstract

PURPOSE OF REVIEW

The clinical overlap between spondyloarthritis (SpA) and inflammation of barrier tissues such as the intestine and skin indicates a role of barrier tissue immunity in the development of SpA. Herein, we review the recent advances in understanding lymphocyte populations and functions within the intestine and skin implicated in the pathophysiology of SpA.

RECENT FINDINGS

A number of unique lymphocyte populations have been identified to be expanded within the gut and skin of patients with SpA, including γδ T cells, mucosa-associated invariant T (MAIT) cells, innate lymphoid cells (ILCs) and T resident memory (TRM) cells. These cells respond to microbial cues at their barrier surface causing cellular activation and generation of interleukin (IL)-17, which is hypothesized to be the mechanism by which they contribute to SpA pathogenesis.

SUMMARY

Understanding how unique lymphocyte populations expand and produce IL-17 in the development of SpA provides insights into the pathophysiology of this disease as well as potential future therapeutic avenues.

摘要

目的综述

脊柱关节炎（SpA）与肠道和皮肤等屏障组织炎症之间的临床重叠表明，屏障组织免疫在 SpA 的发生发展中起作用。在此，我们综述了对 SpA 病理生理学相关的肠道和皮肤内涉及的淋巴细胞群及其功能的最新认识进展。

最近发现

在 SpA 患者的肠道和皮肤内已经确定了许多独特的淋巴细胞群的扩增，包括 γδ T 细胞、黏膜相关不变 T（MAIT）细胞、先天淋巴细胞（ILCs）和组织驻留记忆（TRM）细胞。这些细胞在其屏障表面对微生物信号做出反应，导致细胞激活和白细胞介素（IL）-17 的产生，这被假设是它们导致 SpA 发病机制的机制。

总结

了解独特的淋巴细胞群如何在 SpA 的发展过程中扩增并产生 IL-17，为该疾病的病理生理学提供了深入了解，也为未来的潜在治疗途径提供了思路。