期刊
JOINT BONE SPINE
卷 84, 期 4, 页码 421-426出版社
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.jbspin.2016.07.005
关键词
Anti-inflammatory T cells; Giant cell arteritis; Macrophage; Pro-inflammatory T cells; CD8(+) Treg cells
类别
资金
- National Institutes of Health [R01 AR042527, R01 AI044142, HL 117913, R01 AI108906, R01 AI108891, R01 AG045779, U19 AI057229, U19 AI057266, I01 BX001669]
- Govenard Discovery Fund
Giant cell arteritis is an autoimmune disease defined by explicit tissue tropism to the walls of medium and large arteries. Pathognomic inflammatory lesions are granulomatous in nature, emphasizing the functional role of CD4 T cells and macrophages. Evidence for a pathogenic role of antibodies and immune complexes is missing. Analysis of T cell populations in giant cell arteritis, both in the tissue lesions and in the circulation, has supported a model of broad, polyclonal T cell activation, involving an array of functional T cell lineages. The signature of T cell cytokines produced by vasculitic lesions is typically multifunctional, including IL-2, IFN-gamma, IL-17, IL-21, and GM-CSF, supportive for a general defect in T cell regulation. Recent data describing the lack of a lymph node-based population of anti-inflammatory T cells in giant cell arteritis patients offers a fresh look at the immunopathology of this vasculitis. Due to defective CD8(+)NOX2(+) regulatory T cells, giant cell arteritis patients appear unable to curtail clonal expansion within the CD4 T cell compartment, resulting in widespread CD4 T cell hyperimmunity. Why unopposed expansion of committed CD4 effector T cells would lead to invasion of the walls of medium and large arteries needs to be explored in further investigations. (C) 2016 Societe francaise de rhumatologie. Published by Elsevier Masson SAS. All rights reserved.
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