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本文引用的文献

1
Development of proteoglycan-induced arthritis depends on T cell-supported autoantibody production, but does not involve significant influx of T cells into the joints.蛋白聚糖诱导性关节炎的发展依赖于 T 细胞支持的自身抗体产生,但不涉及 T 细胞大量涌入关节。
Arthritis Res Ther. 2010;12(2):R44. doi: 10.1186/ar2954. Epub 2010 Mar 18.
2
Developments in the scientific understanding of rheumatoid arthritis.类风湿关节炎的科学认识进展。
Arthritis Res Ther. 2009;11(5):249. doi: 10.1186/ar2758. Epub 2009 Oct 14.
3
Abatacept for rheumatoid arthritis.用于类风湿性关节炎的阿巴西普。
Cochrane Database Syst Rev. 2009 Oct 7;2009(4):CD007277. doi: 10.1002/14651858.CD007277.pub2.
4
Arthritis induced by posttranslationally modified (citrullinated) fibrinogen in DR4-IE transgenic mice.DR4-IE转基因小鼠中由翻译后修饰(瓜氨酸化)的纤维蛋白原诱导的关节炎
J Exp Med. 2008 Apr 14;205(4):967-79. doi: 10.1084/jem.20072051. Epub 2008 Apr 7.
5
CD4+ T cells recognizing a single self-peptide expressed by APCs induce spontaneous autoimmune arthritis.识别由抗原呈递细胞(APCs)表达的单一自身肽的CD4 + T细胞会诱发自发性自身免疫性关节炎。
J Immunol. 2008 Jan 15;180(2):833-41. doi: 10.4049/jimmunol.180.2.833.
6
The sphingosine 1-phosphate receptor 1 causes tissue retention by inhibiting the entry of peripheral tissue T lymphocytes into afferent lymphatics.1-磷酸鞘氨醇受体1通过抑制外周组织T淋巴细胞进入输入淋巴管而导致组织滞留。
Nat Immunol. 2008 Jan;9(1):42-53. doi: 10.1038/ni1534. Epub 2007 Nov 25.
7
Animal models of arthritis caused by systemic alteration of the immune system.由免疫系统全身性改变引起的关节炎动物模型。
Curr Opin Immunol. 2005 Dec;17(6):589-94. doi: 10.1016/j.coi.2005.09.017. Epub 2005 Oct 7.
8
Tracking of proinflammatory collagen-specific T cells in early and late collagen-induced arthritis in humanized mice.人源化小鼠早期和晚期胶原诱导性关节炎中促炎胶原特异性T细胞的追踪
J Immunol. 2004 Dec 1;173(11):7037-45. doi: 10.4049/jimmunol.173.11.7037.
9
Immunization with glucose-6-phosphate isomerase induces T cell-dependent peripheral polyarthritis in genetically unaltered mice.用葡萄糖-6-磷酸异构酶进行免疫接种可在基因未改变的小鼠中诱发T细胞依赖性外周多关节炎。
J Immunol. 2004 Apr 1;172(7):4503-9. doi: 10.4049/jimmunol.172.7.4503.
10
Arthritis provoked by linked T and B cell recognition of a glycolytic enzyme.由T细胞和B细胞对一种糖酵解酶的联合识别引发的关节炎
Science. 1999 Nov 26;286(5445):1732-5. doi: 10.1126/science.286.5445.1732.

关节炎:T 细胞在哪里?

Arthritis: where are the T cells?

出版信息

Arthritis Res Ther. 2010;12(3):122. doi: 10.1186/ar3008. Epub 2010 Jun 3.

DOI:10.1186/ar3008
PMID:20537200
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2911865/
Abstract

T-helper (Th) lymphocytes contribute to arthritis pathogenesis by helping B cells to produce antibodies, by producing cytokines that activate effector cells involved in the destruction of cartilage and bone, and by contributing to osteoclast differentiation. There are murine models of arthritis, most notably collagen- and proteoglycan-induced arthritis, in which arthritis depends on T-cell recognition of antigens that are expressed in the joints. In spite of this, we still do not know the antigens recognised by arthritogenic Th cells in humans. Moreover, current evidence for Th cells exerting arthritogenic effector functions within the joints is only indirect.

摘要

辅助性 T 淋巴细胞(Th)通过帮助 B 细胞产生抗体、产生细胞因子激活参与软骨和骨破坏的效应细胞,以及促进破骨细胞分化,有助于关节炎发病机制。有许多关节炎的啮齿动物模型,最显著的是胶原和蛋白聚糖诱导的关节炎,其中关节炎依赖于 T 细胞识别在关节中表达的抗原。尽管如此,我们仍然不知道人类关节炎产生性 Th 细胞识别的抗原。此外,目前关于 Th 细胞在关节中发挥关节炎效应功能的证据只是间接的。