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.
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.
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。
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