Altered signal transduction in SLE T cells

被引:43
作者
Tenbrock, K.
Juang, Y.-T.
Kyttaris, V. C.
Tsokos, G. C.
机构
[1] Univ Hosp Muenster, Div Rheumatol, Dept Pediat, D-48145 Munster, Germany
[2] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Rheumatol, Boston, MA 02115 USA
关键词
lupus; CREM; CamKIV; Elf-1; NFAT; AP-1; SYSTEMIC-LUPUS-ERYTHEMATOSUS; RESPONSE ELEMENT MODULATOR; RECEPTOR ZETA-CHAIN; PROTEIN-KINASE-C; SUPPRESSES IL-2 PRODUCTION; PERIPHERAL-BLOOD; 3'-UNTRANSLATED REGION; DECREASED EXPRESSION; PROMOTER ACTIVITY; DOWN-REGULATION;
D O I
10.1093/rheumatology/kem154
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
T cells from patients with systemic lupus erythematosus display numerous signalling abnormalities. The T cell receptor complex is rewired with the common FcR gamma chain replacing the CD3 zeta chain while the T cell surface membrane lipid rafts are aggregated. These two aberrations result in enhanced early signalling events and altered downstream signalling events. These are in turn responsible for an altered expression of cytokines such as interleukin-6 (IL-6), IL-10, IL-2, IFNy and CD40 ligand. While some of these abnormalities explain the enhanced ability of T cells to help B cells to produce autoantibodies, decreased IL-2 production results in enhanced susceptibility to infections, reduced activation-induced cell death and prolonged survival of autoreactive T cells, which promote help to autoreactive B cells.
引用
收藏
页码:1525 / 1530
页数:6
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