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干燥综合征中的T淋巴细胞:病理生理学的促成因素和调节因子

T lymphocytes in Sjögren's syndrome: contributors to and regulators of pathophysiology.

作者信息

Katsifis Gikas E, Moutsopoulos Niki M, Wahl Sharon M

机构信息

Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892-4352, USA.

出版信息

Clin Rev Allergy Immunol. 2007 Jun;32(3):252-64. doi: 10.1007/s12016-007-8011-8.

Abstract

Sjögren's syndrome is a chronic autoimmune disorder characterized by lymphocytic infiltration and malfunction of the exocrine glands, resulting in dry mouth and eyes. This multigenic and multifunctional disease can present as primary Sjögren's syndrome or secondary to an underlying connective tissue disease. Immune activation subsequent to activation or apoptosis of glandular epithelial cells in genetically predisposed individuals may expose autoantigens, which engage self-perpetuating T cell dependent autoimmune sequelae. The cellular and molecular context of this immune response may drive proinflammatory (Th1 and Th17) and restrain inhibitory (Treg) pathways. Inability to suppress the immune response results in persistent tissue damage and compromised function of salivary and lacrimal glands. Defining the contributions of participating T cells may unravel strategies for therapeutic intervention.

摘要

干燥综合征是一种慢性自身免疫性疾病,其特征为淋巴细胞浸润和外分泌腺功能障碍,导致口干和眼干。这种多基因和多功能疾病可表现为原发性干燥综合征或继发于潜在的结缔组织病。在具有遗传易感性的个体中,腺上皮细胞激活或凋亡后发生的免疫激活可能会暴露自身抗原,从而引发依赖T细胞的自身免疫持续后遗症。这种免疫反应的细胞和分子背景可能会驱动促炎(Th1和Th17)途径并抑制抑制性(Treg)途径。无法抑制免疫反应会导致持续的组织损伤以及唾液腺和泪腺功能受损。明确参与其中的T细胞的作用可能会揭示治疗干预策略。

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