Cloning and characterization of the highly expressed ETEA gene from blood cells of atopic dermatitis patients

被引:17
作者
Imai, Y
Nakada, A
Hashida, R
Sugita, Y
Tanaka, T
Tsujimoto, G
Matsumoto, K
Akasawa, A
Saito, H
Oshida, T
机构
[1] Teikyo Univ, Biotech Ctr, Genox Res Inc, Miyamae Ku, Kanagawa 2160001, Japan
[2] Mie Univ, Sch Med, Dept Mol & Cellular Pharmacol, Tsu, Mie 5140001, Japan
[3] Natl Res Inst Child Hlth & Dev, Tokyo 1548567, Japan
关键词
T cells; ETEA; eosinophils; transcription; atopic dermatitis; expression; Fas; FAF1;
D O I
10.1016/S0006-291X(02)02380-X
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Analysis of patients with atopic dermatitis (AD) for differential expression of genes, as compared to normal individuals, will be useful for understanding the molecular pathogenesis of AD. We found that the expression of the gene ETEA in human peripheral blood CD3-positive cells from patients with atopic dermatitis was significantly higher than in normal individuals. Eosinophils from AD patients expressed ETEA at a significantly higher level than the healthy controls. The overall sequence of the 445 aa deduced polypeptide from the cloned ETEA cDNA showed homology to human Fas-associated factor 1 (FAF1), which is involved in Fas-mediated apoptosis. However, the interaction of ETEA with the Fas death domain was weaker than that of FAF1, as studied in yeast two-hybrid experiments. The ETEA-EGFP fusion protein was expressed in cytoplasm. During the course of activation-induced cell death of primary T cells, transcription levels of ETEA and FAF1 were upregulated with similar kinetics. The enhanced expression of ETEA may play a role in the regulating the resistance to apoptosis that is observed in T cells and eosinophils of AD patients. (C) 2002 Elsevier Science (USA). All rights reserved.
引用
收藏
页码:1282 / 1290
页数:9
相关论文
共 25 条
[1]   A FAS-ASSOCIATED PROTEIN FACTOR, FAF1, POTENTIATES FAS-MEDIATED APOPTOSIS [J].
CHU, KT ;
NIU, XH ;
WILLIAMS, LT .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (25) :11894-11898
[2]   Priming of circulating human eosinophils following late response to allergen challenge [J].
Evans, DJ ;
Lindsay, MA ;
OConnor, BJ ;
Barnes, PJ .
EUROPEAN RESPIRATORY JOURNAL, 1996, 9 (04) :703-708
[3]   DOMINANT INTERFERING FAS GENE-MUTATIONS IMPAIR APOPTOSIS IN A HUMAN AUTOIMMUNE LYMPHOPROLIFERATIVE SYNDROME [J].
FISHER, GH ;
ROSENBERG, FJ ;
STRAUS, SE ;
DALE, JK ;
MIDDELTON, LA ;
LIN, AY ;
STROBER, W ;
LENARDO, MJ ;
PUCK, JM .
CELL, 1995, 81 (06) :935-946
[4]   Mechanisms of eosinophil-associated inflammation [J].
Gleich, GJ .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2000, 105 (04) :651-663
[5]   A role for Th1 and Th2 cells in the immunopathogenesis of atopic dermatitis [J].
Grewe, M ;
Bruijnzeel-Koomen, CAFM ;
Schöpf, E ;
Thepen, T ;
Langeveld-Wildschut, AG ;
Ruzicka, T ;
Krutmann, J .
IMMUNOLOGY TODAY, 1998, 19 (08) :359-361
[6]  
Guerra B, 2001, INT J ONCOL, V19, P1117
[7]   Disruption of Fas receptor signaling by nitric oxide in eosinophils [J].
Hebestreit, H ;
Dibbert, B ;
Balatti, I ;
Braun, D ;
Schapowal, A ;
Blaser, K ;
Simon, HU .
JOURNAL OF EXPERIMENTAL MEDICINE, 1998, 187 (03) :415-425
[8]  
Jayaraman S, 1999, J IMMUNOL, V162, P1717
[9]   Phosphorylation of the Fas associated factor FAF1 by protein kinase CK2 and identification of serines 289 and 291 as the in vitro phosphorylation sites [J].
Jensen, HH ;
Hjerrild, M ;
Guerra, B ;
Larsen, MR ;
Hojrup, P ;
Boldyreff, B .
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, 2001, 33 (06) :577-589
[10]   ACTIVATION-INDUCED CELL-DEATH (APOPTOSIS) OF MATURE PERIPHERAL T-LYMPHOCYTES [J].
KABELITZ, D ;
POHL, T ;
PECHHOLD, K .
IMMUNOLOGY TODAY, 1993, 14 (07) :338-338