Gene expression profile of CD4+T cells reveals an interferon signaling suppression associated with progression of experimental Schistosoma japonicum infection

被引:17
作者
Ji, MJ [1 ]
Su, C [1 ]
Wu, HW [1 ]
Zhu, X [1 ]
Cai, XP [1 ]
Li, CL [1 ]
Li, GF [1 ]
Wang, Y [1 ]
Zhang, ZS [1 ]
Wu, GL [1 ]
机构
[1] Nanjing Med Univ, Res Lab, Nanjing 210029, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
Schistosoma japonicwn; CD4(+) T cell; oligonucleotide microarray; interferons; interferon-inducible gene; interferon-gamma-regulated GTPase family;
D O I
10.1016/j.cellimm.2003.08.001
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
To understand the natural history of immune responses centering CD4(+) T cells at genetic level during experimental infection with Schistosoma japonicum (S. japonicum), the mRNA profiles of CD4+ T cells from spleens of mice at 0, 3, 6, and 13 weeks after the onset of the infection, were compared using mouse oliogonucleotide microarrays (Affymetrix GeneChip U74A). Of about 12,000 mouse probe sets in a microarray, nearly 10% encoded a variety of immune regulators, including many cytokine and chemokine genes, immuno globulin-related genes, and genes related to apoptosis and the stress response. These changed in transcript representation as the schistosome infection progressed, and a key finding, which was validated by semi-quantitative PCR, was that a significant portion of the genes which were down-regulated as infection progressed coded for interferon (IFN)-inducible molecules, including GTPases, transcription factors and chemokines. The results thus showed that there is a characteristic change in IFN-inducible gene expression over the course of the schistosome infection, and it is suggested that the IFN-gamma-regulated GTPase family may be involved in IFN-mediated resistance against S. japonicum. (C) 2003 Elsevier Inc. All rights reserved.
引用
收藏
页码:55 / 62
页数:8
相关论文
共 24 条
[1]  
Anderson S, 1999, IMMUNOLOGY, V96, P22, DOI 10.1046/j.1365-2567.1999.00661.x
[2]   Schistosomiasis vaccines: Research to development [J].
Bergquist, NR ;
Colley, DG .
PARASITOLOGY TODAY, 1998, 14 (03) :99-104
[3]   Inactivation of LRG-47 and IRG-47 reveals a family of interferon γ-inducible genes with essential, pathogen-specific roles in resistance to infection [J].
Collazo, CM ;
Yap, GS ;
Sempowski, GD ;
Lusby, KC ;
Tessarollo, L ;
Woude, GFV ;
Sher, A ;
Taylor, GA .
JOURNAL OF EXPERIMENTAL MEDICINE, 2001, 194 (02) :181-187
[4]   HUMAN IGE, IGG4 AND RESISTANCE TO REINFECTION WITH SCHISTOSOMA-HAEMATOBIUM [J].
HAGAN, P ;
BLUMENTHAL, UJ ;
DUNN, D ;
SIMPSON, AJG ;
WILKINS, HA .
NATURE, 1991, 349 (6306) :243-245
[5]   EOSINOPHILIA AND RESISTANCE TO SCHISTOSOMA-HAEMATOBIUM IN MAN [J].
HAGAN, P ;
WILKINS, HA ;
BLUMENTHAL, UJ ;
HAYES, RJ ;
GREENWOOD, BM .
PARASITE IMMUNOLOGY, 1985, 7 (06) :625-632
[6]   Interferon consensus sequence binding protein confers resistance against Yersinia enterocolitica [J].
Hein, J ;
Kempf, VAJ ;
Diebold, J ;
Bücheler, N ;
Preger, S ;
Horak, I ;
Sing, A ;
Kramer, U ;
Autenrieth, IB .
INFECTION AND IMMUNITY, 2000, 68 (03) :1408-1417
[7]   Disease fingerprinting with cDNA microarrays reveals distinct gene expression profiles in lethal type-1 and type-2 cytokine-mediated inflammatory reactions [J].
Hoffmann, KF ;
McCarty, TC ;
Segal, DH ;
Chiaramonte, M ;
Hesse, M ;
Davis, EM ;
Cheever, AW ;
Meltzer, PS ;
Morse, HC ;
Wynn, TA .
FASEB JOURNAL, 2001, 15 (11) :2545-+
[8]   Susceptibility of IFN regulatory factor-1 and IFN consensus sequence binding protein-deficient mice to brucellosis [J].
Ko, J ;
Gendron-Fitzpatrick, A ;
Splitter, GA .
JOURNAL OF IMMUNOLOGY, 2002, 168 (05) :2433-2440
[9]   ICSBP/IRF-8 transactivation: A tale of protein-protein interaction [J].
Levi, BZ ;
Hashmueli, S ;
Gleit-Kielmanowicz, M ;
Azriel, A ;
Meraro, D .
JOURNAL OF INTERFERON AND CYTOKINE RESEARCH, 2002, 22 (01) :153-160
[10]   Stimulation of IRF-7 gene expression by tumor necrosis factor α -: Requirement for NFκB transcription factor and gene accessibility [J].
Lu, RQ ;
Moore, PA ;
Pitha, PM .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (19) :16592-16598