Potential role of CagA in the inhibition of T cell reactivity in Helicobacter pylori infections

被引:59
作者
Paziak-Domanska, B [1 ]
Chmiela, M [1 ]
Jarosinska, A [1 ]
Rudnicka, W [1 ]
机构
[1] Univ Lodz, Dept Infect Biol, Inst Microbiol & Immunol, PL-90237 Lodz, Poland
关键词
Helicobacter pylori; CagA; T cell proliferation;
D O I
10.1006/cimm.2000.1654
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The pathogenicity of chronic gastroduodenal diseases is very often related to Helicobacter pylori infections. Most H. pylori strains carry the cagA gene encoding an immunodominant 120- to 128-kDa protein which is considered a virulence marker. The majority of CagA-positive H. pylori isolates also produce a 95-kDa protein cytotoxin (VacA) causing vacuolation and degradation of mammalian cells. In our previous study we have shown that live H. pylori bacteria and their sonicates inhibit PHA-driven proliferation of human T lymphocytes. The H. pylori CagA and VacA proteins were suspected of a paralyzing effect of H. pylori on T cell proliferation. In this report, by using isogenic H. pylori mutant strains defective in CagA and VacA proteins, we determined that CagA is responsible for the inhibition of PHA-induced proliferation of T cells. (C) 2000 Academic Press.
引用
收藏
页码:136 / 139
页数:4
相关论文
共 27 条
[1]   Analyses of the cag pathogenicity island of Helicobacter pylori [J].
Akopyants, NS ;
Clifton, SW ;
Kersulyte, D ;
Crabtree, JE ;
Youree, BE ;
Reece, CA ;
Bukanov, NO ;
Drazek, ES ;
Roe, BA ;
Berg, DE .
MOLECULAR MICROBIOLOGY, 1998, 28 (01) :37-53
[2]  
Atherton JC, 1998, BRIT MED BULL, V54, P105
[3]  
BAMFORD KB, 1997, IRISH J MED SCI, V166, P3
[4]   cag, a pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-associated virulence factors [J].
Censini, S ;
Lange, C ;
Xiang, ZY ;
Crabtree, JE ;
Ghiara, P ;
Borodovsky, M ;
Rappuoli, R ;
Covacci, A .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (25) :14648-14653
[5]   The proliferation of human T lymphocytes stimulated by Helicobacter pylori antigens [J].
Chmiela, M ;
PaziakDomanska, B ;
Ljungh, A ;
Wadstrom, T ;
Rudnicka, W .
IMMUNOBIOLOGY, 1996, 195 (02) :199-208
[6]  
Chmiela M, 1996, J PHYSIOL PHARMACOL, V47, P195
[7]   The vacuolating cytotoxin of Helicobacter pylori [J].
Cover, TL .
MOLECULAR MICROBIOLOGY, 1996, 20 (02) :241-246
[8]   Eradication of chronic Helicobacter pylori infection by therapeutic vaccination [J].
Crabtree, JE .
GUT, 1998, 43 (01) :7-8
[9]   Detection of serum antibodies to CagA and VacA and of serum neutralizing activity for vacuolating cytotoxin inpatients with Helicobacter pylori-induced gastritis [J].
Donati, M ;
Moreno, S ;
Storni, E ;
Tucci, A ;
Poli, L ;
Mazzoni, C ;
Varoli, O ;
Sambri, V ;
Farencena, A ;
Cevenini, R .
CLINICAL AND DIAGNOSTIC LABORATORY IMMUNOLOGY, 1997, 4 (04) :478-482
[10]   Immunization of mice with urease vaccine affords protection against Helicobacter pylori infection in the absence of antibodies and is mediated by MHC class II-restricted responses [J].
Ermak, TH ;
Giannasca, PJ ;
Nichols, R ;
Myers, GA ;
Nedrud, J ;
Weltzin, R ;
Lee, CK ;
Kleanthous, H ;
Monath, TP .
JOURNAL OF EXPERIMENTAL MEDICINE, 1998, 188 (12) :2277-2288