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Engagement of glucocorticoid-induced TNF receptor costimulates NKT cell activation in vitro and in vivo.糖皮质激素诱导的肿瘤坏死因子受体的参与在体外和体内共同刺激NKT细胞活化。
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Natural killer T (NKT) cells attenuate bleomycin-induced pulmonary fibrosis by producing interferon-gamma.自然杀伤性T（NKT）细胞通过产生γ干扰素减轻博来霉素诱导的肺纤维化。
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NKT cells promote antibody-induced joint inflammation by suppressing transforming growth factor beta1 production.自然杀伤T细胞通过抑制转化生长因子β1的产生来促进抗体诱导的关节炎症。
J Exp Med. 2005 Jan 3;201(1):41-7. doi: 10.1084/jem.20041400.
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Colony-stimulating factor-1-dependent macrophages are responsible for IVIG protection in antibody-induced autoimmune disease.集落刺激因子-1依赖性巨噬细胞在抗体诱导的自身免疫性疾病中负责静脉注射免疫球蛋白的保护作用。
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NKT cells inhibit the onset of diabetes by impairing the development of pathogenic T cells specific for pancreatic beta cells.自然杀伤T细胞通过损害胰腺β细胞特异性致病性T细胞的发育来抑制糖尿病的发生。
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FcγRIII的结合在抗体诱导的关节炎症中为NKT细胞提供激活信号。

FcgammaRIII engagement provides activating signals to NKT cells in antibody-induced joint inflammation.

作者信息

Kim Hye Young, Kim Sanghee, Chung Doo Hyun

机构信息

Department of Pathology, Graduate Program of Immunology, Seoul National University College of Medicine, Seoul, Republic of Korea.

出版信息

J Clin Invest. 2006 Sep;116(9):2484-92. doi: 10.1172/JCI27219. Epub 2006 Aug 17.

DOI:10.1172/JCI27219
PMID:16917543
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1550276/
Abstract

NKT cells promote antibody-induced arthritis, but the mechanism by which NKT cells are activated in this model remains unclear. It has been proposed that Fcgamma receptor (FcgammaR) contributes to NKT cell activation in antibody-induced arthritis. To address this issue, we explored the functions of FcgammaR on NKT cells in antibody-induced arthritis. RT-PCR and flow cytometric analysis demonstrated that NKT cells constitutively express surface FcgammaRIII but not FcgammaRI, -II, or -IV. FcgammaRIII engagement by aggregated IgG on NKT cells enhanced CD25 and CD69 expression, whereas FcgammaR(-/-) mouse NKT cells did not enhance activation. FcgammaRIII engagement on NKT cells enhanced the production of IL-4, IL-10, IL-13, and IFN-gamma, whereas FcgammaR-deficient NKT cells did not alter the production of these cytokines after aggregated IgG treatment. However, FcgammaR-deficient NKT cells were functionally intact in terms of TCR-induced activation. Moreover, adoptive transfer of FcgammaR-deficient NKT cells could not restore inflammation or TGF-beta production in the joint tissues of CD1d(-/-) mice, whereas adoptive transfer of wild-type NKT cells induced arthritis and reduced TGF-beta production in joint tissues. We conclude that FcgammaRIII engagement by IgG in joint tissues provides activating signals to NKT cells in antibody-induced arthritis.

摘要

NKT细胞可促进抗体诱导的关节炎，但在该模型中NKT细胞被激活的机制仍不清楚。有人提出，Fcγ受体（FcγR）在抗体诱导的关节炎中有助于NKT细胞的激活。为解决这一问题，我们探讨了FcγR在抗体诱导的关节炎中对NKT细胞的功能。逆转录聚合酶链反应（RT-PCR）和流式细胞术分析表明，NKT细胞组成性表达表面FcγRIII，但不表达FcγRI、-II或-IV。NKT细胞上聚集的IgG与FcγRIII结合可增强CD25和CD69的表达，而FcγR（-/-）小鼠的NKT细胞则不会增强激活。NKT细胞上FcγRIII的结合可增强IL-4、IL-10、IL-13和IFN-γ的产生，而FcγR缺陷的NKT细胞在聚集IgG处理后不会改变这些细胞因子的产生。然而，FcγR缺陷的NKT细胞在TCR诱导的激活方面功能完整。此外，FcγR缺陷的NKT细胞的过继转移不能恢复CD1d（-/-）小鼠关节组织中的炎症或TGF-β的产生，而野生型NKT细胞的过继转移则会诱导关节炎并降低关节组织中TGF-β的产生。我们得出结论，关节组织中IgG与FcγRIII的结合为抗体诱导的关节炎中的NKT细胞提供了激活信号。