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OPN 调控的 CEACAM1 表达在促进口腔扁平苔藓患者活化 T 细胞存活和口腔角质形成细胞凋亡中的可能作用。

The possible roles of OPN-regulated CEACAM1 expression in promoting the survival of activated T cells and the apoptosis of oral keratinocytes in oral lichen planus patients.

机构信息

Department of Pathology, Stomatology College of Shandong University, 44-1#, Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China.

出版信息

J Clin Immunol. 2011 Oct;31(5):827-39. doi: 10.1007/s10875-011-9552-4. Epub 2011 Jun 14.

DOI:10.1007/s10875-011-9552-4
PMID:21671129
Abstract

Oral lichen planus is a chronic inflammatory disorder of the oral mucosa that represents T cell-mediated autoimmune diseases. The regulation and roles of carcinoembryonic antigen-related cellular adhesion molecule 1 (CEACAM1), a novel immune molecule, in the immunopathogenesis of T cell-mediated autoimmune diseases remain unclear. In the current paper, CEACAM1 was found to be overexpressed in peripheral T cells and epithelial cells in oral lichen planus patients. A fraction of infiltrating inflammatory mononuclear cells in the lamina propria of the oral lichen planus mucosa also expressed CEACAM1. Importantly, for the first time, CEACAM1 expression in T cells and in normal human oral keratinocytes was demonstrated to be regulated differently by osteopontin in vitro. Furthermore, the apoptosis of oral keratinocytes and activated T cells can be markedly suppressed by CEACAM1-specific monoclonal antibodies. In conclusion, OPN-regulated CEACAM1 expression may play a critical role in the immunopathogenesis of oral lichen planus.

摘要

口腔扁平苔藓是一种口腔黏膜的慢性炎症性疾病,代表 T 细胞介导的自身免疫性疾病。癌胚抗原相关细胞黏附分子 1(CEACAM1)是一种新型免疫分子,其在 T 细胞介导的自身免疫性疾病的免疫发病机制中的调节和作用尚不清楚。在本论文中,发现 CEACAM1 在口腔扁平苔藓患者的外周 T 细胞和上皮细胞中过度表达。口腔扁平苔藓黏膜固有层中浸润的炎症性单核细胞的一部分也表达 CEACAM1。重要的是,首次证明骨桥蛋白在体外可调节 T 细胞和正常人口腔角质形成细胞中 CEACAM1 的表达。此外,口腔角质形成细胞和活化 T 细胞的凋亡可以被 CEACAM1 特异性单克隆抗体显著抑制。总之,OPN 调节的 CEACAM1 表达可能在口腔扁平苔藓的免疫发病机制中起关键作用。

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本文引用的文献

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Blockade of osteopontin reduces alloreactive CD8+ T cell-mediated graft-versus-host disease.阻断骨桥蛋白可减少同种异体反应性 CD8+T 细胞介导的移植物抗宿主病。
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[Significance of cell immunoreactions and cell apoptosis in oral lichen planus].
由于缺乏癌胚抗原相关细胞黏附分子(CEACAM)受体表达,导致空泡毒素相关蛋白A(CagA)无法分泌到口腔上皮细胞中。
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Effect of CEACAM-1 knockdown in human colorectal cancer cells.癌胚抗原相关细胞黏附分子1(CEACAM-1)基因敲低对人结肠癌细胞的影响。
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Loss of CEACAM1, a Tumor-Associated Factor, Attenuates Post-infarction Cardiac Remodeling by Inhibiting Apoptosis.肿瘤相关因子CEACAM1的缺失通过抑制细胞凋亡减轻心肌梗死后的心脏重塑。
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Hua Xi Kou Qiang Yi Xue Za Zhi. 2009 Jun;27(3):256-9.
4
Defect in CEACAM family member expression in Crohn's disease IECs is regulated by the transcription factor SOX9.CEACAM 家族成员在克罗恩病 IEC 中的表达缺陷受转录因子 SOX9 调控。
Inflamm Bowel Dis. 2009 Dec;15(12):1775-83. doi: 10.1002/ibd.21023. Epub 2009 Jul 27.
5
Pivotal advance: CEACAM1 is a negative coreceptor for the B cell receptor and promotes CD19-mediated adhesion of B cells in a PI3K-dependent manner.关键进展:癌胚抗原相关细胞黏附分子1(CEACAM1)是B细胞受体的负性共受体,并以磷脂酰肌醇-3-激酶(PI3K)依赖的方式促进CD19介导的B细胞黏附。
J Leukoc Biol. 2009 Aug;86(2):205-18. doi: 10.1189/jlb.0109037. Epub 2009 May 19.
6
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J Invest Dermatol. 2009 May;129(5):1140-8. doi: 10.1038/jid.2008.350. Epub 2008 Nov 20.
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