Abnormal early TCR/CD3-mediated signaling events of a snRNP-autoreactive lupus T cell clone

被引:17
作者
Liossis, SNC
Hoffman, RW
Tsokos, GC
机构
[1] Uniformed Serv Univ Hlth Sci, Dept Med, Bethesda, MD 20814 USA
[2] Univ Missouri, Dept Internal Med, Div Rheumatol & Immunol, Columbia, MO 65212 USA
[3] Vet Adm Med Ctr, Columbia, MO 65212 USA
[4] Walter Reed Army Med Ctr, Walter Reed Army Inst Res, Dept Clin Pathol, Washington, DC 20307 USA
来源
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY | 1998年 / 88卷 / 03期
关键词
systemic lupus erythematosus; signal transduction; autoantigen; antigen receptor; snRNP;
D O I
10.1006/clin.1998.4569
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Multiple immunoregulatory abnormalities characterize systemic lupus erythematosus. Abnormalities of the antigen receptor-mediated early signal transduction biochemical events underscore the diverse cellular aberrations. Fresh peripheral T and B cells and T cell lines from patients with systemic lupus erythematosus display increased Ca2+ responses that are preceded by enhanced antigen receptor-initiated cytosolic protein tyrosine phosphorylation. To further dissect the aberrant signaling events of lupus T cells we studied the early anti-CD3 mAb-induced signaling events in autoantigen-specific T cells from lupus patients. We report herein that a lupus snRNP-specific T cell clone, but not other T cells, displays increased Ca2+ fluxes and enhanced production of tyrosine-phosphorylated proteins following TCR/CD3 stimulation.
引用
收藏
页码:305 / 310
页数:6
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