Helicobacter pylori phase variation, immune modulation and gastric autoimmunity

被引：78

作者：

Bergman, M

Del Prete, G

van Kooyk, Y

Appelmelk, B

机构：

[1] Erasmus Univ, Med Ctr, Dept Med Microbiol & Infect Dis, NL-3015 GD Rotterdam, Netherlands

[2] Univ Florence, Dept Internal Med, I-50134 Florence, Italy

[3] Free Univ Amsterdam, Med Ctr, Dept Mol Cell Biol & Immunol, NL-1081 BT Amsterdam, Netherlands

[4] Free Univ Amsterdam, Med Ctr, Dept Med Microbiol & Infect Control, NL-1081 BT Amsterdam, Netherlands

来源：

NATURE REVIEWS MICROBIOLOGY | 2006年 / 4卷 / 02期

关键词：

D O I：

10.1038/nrmicro1344

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Helicobacter pylori can be regarded as a model pathogen for studying persistent colonization of humans. Phase-variable expression of Lewis blood-group antigens by H. pylori allows this microorganism to modulate the host T-helper-1-cell versus T-helper-2-cell response. We describe a model in which interactions between host lectins and pathogen carbohydrates facilitate asymptomatic persistence of H. pylori. This delicate balance, favourable for both the pathogen and the host, could lead to gastric autoimmunity in genetically susceptible individuals.

引用

收藏

页码：151 / 159

页数：10

相关论文

共 89 条

[11] Helicobacter pylori modulates the T helper cell 1/T helper cell 2 balance through phase-variable interaction between lipopolysaccharide and DC-SIGN [J].

Bergman, MP ;

Engering, A ;

Smits, HH ;

van Vliet, SJ ;

van Bodegraven, AA ;

Wirth, HP ;

Kapsenberg, ML ;

Vandenbroucke-Grauls, CMJE ;

van Kooyk, Y ;

Appelmelk, BJ .

JOURNAL OF EXPERIMENTAL MEDICINE, 2004, 200 (08) :979-990

[12] Local transgenic expression of granulocyte macrophage-colony stimulating factor initiates autoimmunity [J].

Biondo, M ;

Nasa, Z ;

Marshall, A ;

Toh, BH ;

Alderuccio, F .

JOURNAL OF IMMUNOLOGY, 2001, 166 (03) :2090-2099

[13]

Blaser MJ, 2004, J CLIN INVEST, V113, P321, DOI [10.1172/JCI200420925, 10.1172/JCI20925]

[14] Hypothesis:: The changing relationships of Helicobacter pylori and humans:: Implications for health and disease [J].

Blaser, MJ .

JOURNAL OF INFECTIOUS DISEASES, 1999, 179 (06) :1523-1530

[15] Helicobacter pylori genetic diversity and risk of human disease [J].

Blaser, MJ ;

Berg, DE .

JOURNAL OF CLINICAL INVESTIGATION, 2001, 107 (07) :767-773

[16] Dectin-1 mediates the biological effects of β-glucans [J].

Brown, GD ;

Herre, J ;

Williams, DL ;

Willment, JA ;

Marshall, ASJ ;

Gordon, S .

JOURNAL OF EXPERIMENTAL MEDICINE, 2003, 197 (09) :1119-1124

[17] How C-type lectins detect pathogens [J].

Cambi, A ;

Koopman, M ;

Figdor, CG .

CELLULAR MICROBIOLOGY, 2005, 7 (04) :481-488

[18] Initiation of autoimmunity [J].

Christen, U ;

von Herrath, MG .

CURRENT OPINION IN IMMUNOLOGY, 2004, 16 (06) :759-767

[19] The gastric H+,K+-ATPase is a major autoantigen in chronic Helicobacter pylori gastritis with body mucosa atrophy [J].

Claeys, D ;

Faller, G ;

Appelmelk, BJ ;

Negrini, R ;

Kirchner, T .

GASTROENTEROLOGY, 1998, 115 (02) :340-347

[20] H+,K+-ATPase (proton pump) is the target autoantigen of Th1-type cytotoxic T cells in autoimmune gastritis [J].

D'Elios, MM ;

Bergman, MP ;

Azzurri, A ;

Amedei, A ;

Benagiano, M ;

De Pont, JJ ;

Cianchi, F ;

Vandenbroucke-Grauls, CM ;

Romagnani, S ;

Appelmelk, BJ ;

Del Prete, G .

GASTROENTEROLOGY, 2001, 120 (02) :377-386

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