Immune modulation and modulators in Heligmosomoides polygyrus infection

被引:101
作者
Maizels, Rick M. [1 ]
Hewitson, James P. [1 ]
Murray, Janice [1 ]
Harcus, Yvonne M. [1 ]
Dayer, Blaise [1 ]
Filbey, Kara J. [1 ]
Grainger, John R. [1 ]
McSorley, Henry J. [1 ]
Reynolds, Lisa A. [1 ]
Smith, Katherine A. [1 ]
机构
[1] Univ Edinburgh, Inst Immunol & Infect Res, Edinburgh EH9 3JT, Midlothian, Scotland
关键词
Alternatively activated macrophages; Antibody isotype; Cytokine; Dendritic cell; Immunosuppression; Mucosal immunity; Secreted immunomodulators; T cell subsets; REGULATORY T-CELLS; ALTERNATIVELY ACTIVATED MACROPHAGES; EGG-INDUCED IMMUNOPATHOLOGY; GASTROINTESTINAL NEMATODE INFECTION; EXCRETORY-SECRETORY PRODUCTS; BLOOD-STAGE MALARIA; NEMATOSPIROIDES-DUBIUS; HELMINTH INFECTION; DENDRITIC CELLS; TGF-BETA;
D O I
10.1016/j.exppara.2011.08.011
中图分类号
R38 [医学寄生虫学]; Q [生物科学];
学科分类号
07 ; 0710 ; 09 ; 100103 ;
摘要
The intestinal nematode parasite Heligmosomoides polygyrus bakeri exerts widespread immunomodulatory effects on both the innate and adaptive immune system of the host. Infected mice adopt an immunoregulated phenotype, with abated allergic and autoimmune reactions. At the cellular level, infection is accompanied by expanded regulatory T cell populations, skewed dendritic cell and macrophage phenotypes, B cell hyperstimulation and multiple localised changes within the intestinal environment. In most mouse strains, these act to block protective Th2 immunity. The molecular basis of parasite interactions with the host immune system centres upon secreted products termed HES (H. polygyrus excretory-secretory antigen), which include a TGF-beta-like ligand that induces de novo regulatory T cells, factors that modify innate inflammatory responses, and molecules that block allergy in vivo. Proteomic and transcriptomic definition of parasite proteins, combined with biochemical identification of immunogenic molecules in resistant mice, will provide new candidate immunomodulators and vaccine antigens for future research. (c) 2011 Elsevier Inc. All rights reserved.
引用
收藏
页码:76 / 89
页数:14
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