Alterations in the expression of signal-transducing CD3ζ chain in T cells from patients with chronic inflammatory/autoimmune diseases

被引：19

作者：

Ciszak, Lidia ^{[1
]}

Pawlak, Edyta ^{[1
]}

Kosmaczewska, Agata ^{[1
]}

Potoczek, Stanislaw ^{[2
]}

Frydecka, Irena ^{[1
,2
]}

机构：

[1] Polish Acad Sci, Inst Immunol & Expt Therapy, Dept Expt Therapy, Immunopathol Lab, PL-53114 Wroclaw, Poland

[2] Wroclaw Med Univ, Dept Hematol, Wroclaw, Poland

来源：

ARCHIVUM IMMUNOLOGIAE ET THERAPIAE EXPERIMENTALIS | 2007年 / 55卷 / 06期

关键词：

CD3 zeta chain; TCR/CD3; complex; chronic inflammatory diseases; autoimmune diseases; SYSTEMIC-LUPUS-ERYTHEMATOSUS; RECEPTOR ZETA-CHAIN; IDIOPATHIC NEPHROTIC SYNDROME; RHEUMATOID-ARTHRITIS PATIENTS; SPLICED 3'-UNTRANSLATED REGION; SYNOVIAL-FLUID LYMPHOCYTES; PERIPHERAL-BLOOD LYMPHOCYTES; HIGH-AFFINITY RECEPTOR; TCR-ZETA; MESSENGER-RNA;

D O I：

10.1007/s00005-007-0042-6

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The CD3 zeta chain, a component of the T cell receptor (TCR)/CD3 complex, is considered to be a limiting factor in the assembly and transport of the TCR/CD3 complex to the cell surface and is crucial to receptor signaling function. Recent studies have demonstrated altered expression and function of this signal transduction molecule in T and natural killer cells in patients with chronic inflammatory/autoimmune diseases. In this review, current knowledge concerning the expression of CD3 zeta chain as well as the mechanisms responsible for abnormal expression of this molecule in systemic lupus erythematosus, rheumatoid arthritis, and childhood idiopathic nephrotic syndrome are summarized.

引用

页码：373 / 386

页数：14

共 118 条

[1] INVITRO MITOGEN STIMULATION OF SYNOVIAL-FLUID LYMPHOCYTES FROM RHEUMATOID-ARTHRITIS AND JUVENILE RHEUMATOID-ARTHRITIS PATIENTS - DISSOCIATION BETWEEN RESPONSE TO ANTIGENS AND POLYCLONAL MITOGENS [J].

ABRAHAMSEN, TG ;

FROLAND, SS ;

NATVIG, JB .

SCANDINAVIAN JOURNAL OF IMMUNOLOGY, 1978, 7 (01) :81-90

[2] Genetic models: clues for understanding the pathogenesis of idiopathic nephrotic syndrome [J].

Antignac, C .

JOURNAL OF CLINICAL INVESTIGATION, 2002, 109 (04) :447-449

[3] A case of unfulfilled expectations. Cytokines in idiopathic minimal lesion nephrotic syndrome [J].

Araya, CE ;

Wasserfall, CH ;

Brusko, TM ;

Mu, W ;

Segal, MS ;

Johnson, RJ ;

Garin, EH .

PEDIATRIC NEPHROLOGY, 2006, 21 (05) :603-610

[4] DO CIRCULATING FACTORS PLAY A ROLE IN THE PATHOGENESIS OF MINIMAL CHANGE NEPHROTIC SYNDROME [J].

BAKKER, WW ;

VANLUIJK, WHJ .

PEDIATRIC NEPHROLOGY, 1989, 3 (03) :341-349

[5] Down-regulation of the T cell receptor CD3ζ chain in rheumatoid arthritis (RA) and its influence on T cell responsiveness [J].

Berg, L ;

Rönnelid, J ;

Klareskog, L ;

Bucht, A .

CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 2000, 120 (01) :174-182

[6]

Brundula V, 1999, ARTHRITIS RHEUM-US, V42, P1908, DOI 10.1002/1529-0131(199909)42:9<1908::AID-ANR17>3.0.CO

[7]

2-7

[8] Prevalence of Fc-gammaR chain expression in CD4+ T cells of patients with systemic lupus erythematosus [J].

Butkiewicz, L ;

Duriagin, S ;

Laddach, R ;

Chwalinska-Sadowska, H ;

Jagodzinski, PP .

SCANDINAVIAN JOURNAL OF RHEUMATOLOGY, 2005, 34 (03) :216-219

[9] Molecular mechanisms for the assembly of the T cell receptor-CD3 complex [J].

Call, ME ;

Wucherpfennig, KW .

MOLECULAR IMMUNOLOGY, 2004, 40 (18) :1295-1305

[10] T cell antigen receptor signal transduction pathways [J].

Cantrell, D .

ANNUAL REVIEW OF IMMUNOLOGY, 1996, 14 :259-274

← 1 2 3 4 5 6 7 8 9 10 →