t细胞免疫球蛋白和粘蛋白结构域3在类风湿关节炎中上调,但在控制炎症方面不足。

IF 1.4 Q4 IMMUNOLOGY American journal of clinical and experimental immunology Pub Date : 2022-06-15 eCollection Date: 2022-01-01
Caecilie Skejoe, Aida S Hansen, Kristian Stengaard-Pedersen, Peter Junker, Kim Hoerslev-Pedersen, Merete L Hetland, Mikkel Oestergaard, Stinne Greisen, Malene Hvid, Mette Deleuran, Bent Deleuran
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摘要

目的:类风湿关节炎(RA)是一种慢性自身免疫性疾病,涉及促炎和抗炎机制。本研究的目的是探讨t细胞免疫球蛋白和粘蛋白结构域3 (Tim-3)在RA中的作用。方法:从前瞻性收集的生物库(clinicaltrials.gov (NCT00660647))获取早期RA (n=98)患者血浆可溶性Tim-3水平,以评估其与治疗和疾病活动度的关系。我们还研究了单独或联合中和抗程序性细胞死亡蛋白1 (PD-1)抗体后,Tim-3对RA患者滑液单核细胞(SFMC)自发细胞因子产生的影响。结果:长期刺激的CD4 t细胞Tim-3表达水平较高,而PD-1表达水平有降低的趋势。Tim-3仅在炎症关节炎关节的CD3、CD4、CD45RO阳性细胞中与PD-1共表达。在RA的SFMC培养物中,加入中和Tim-3抗体可增加IFNγ和MCP-1的分泌。而中和抗pd -1抗体对细胞因子产生更广泛的影响。最后,我们观察到可溶性Tim-3在血浆中增加,并且与早期RA的疾病活动性有关。结论:综上所述,我们的研究结果表明Tim-3在RA中具有疾病抑制作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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T-cell immunoglobulin and mucin domain 3 is upregulated in rheumatoid arthritis, but insufficient in controlling inflammation.

Objectives: Rheumatoid arthritis (RA) is a chronic autoimmune disease, that involves both pro- and anti-inflammatory mechanisms. The purpose of the present study is to investigate T-cell immunoglobulin and mucin domain 3 (Tim-3) in RA.

Methods: Plasma levels of soluble (s) Tim-3 in early RA (n=98), were followed, to evaluate association with treatment and disease activity, acquired from a prospective collected biobank (clinicaltrials.gov (NCT00660647)). We also investigate the influence of Tim-3 on spontaneous cytokine production in synovial fluid mononuclear cells (SFMC) from RA patients after addition of neutralizing anti-Tim-3's antibodies, either alone or in combination with neutralizing anti-Programmed Cell death protein 1 (PD-1) antibodies.

Results: Long-time stimulated CD4 T-cells expressed high levels of Tim-3, but tended to decrease their PD-1 expression. Tim-3 expression was exclusively seen co-expressed with PD-1 by CD3, CD4, CD45RO positive cells in the inflamed RA joint. Addition of neutralizing Tim-3 antibodies increased the secretion of IFNγ and MCP-1, in SFMC cultures from RA. Whereas neutralizing anti-PD-1 antibodies showed a broader impact on cytokine production. Finally, we observed that soluble Tim-3 is increased in plasma and is associated with disease activity in early RA.

Conclusion: Taken together, our findings indicate disease-suppressive functions of Tim-3 in RA.

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