The mechanisms behind helminth's immunomodulation in autoimmunity

被引:49
作者
Bashi, Tomer [1 ]
Bizzaro, Giorgia [1 ]
Shor, Dana Ben-Ami [1 ,2 ]
Blank, Miri [1 ]
Shoenfeld, Yehuda [1 ,3 ]
机构
[1] Tel Aviv Univ, Sackler Fac Med, Sheba Med Ctr, Zabludowicz Ctr Autoimmune Dis, IL-69978 Tel Aviv, Israel
[2] Tel Aviv Univ, Sackler Fac Med, Sheba Med Ctr, Dept Gastroenterol, IL-69978 Tel Aviv, Israel
[3] Tel Aviv Univ, Incumbent Laura Schwarz Kip Chair Res Autoimmune, IL-69978 Tel Aviv, Israel
关键词
Helminths; Autoimmune diseases; Immune system; Mechanisms; Inflammation; Cytokines; NEMATODE-SECRETED PRODUCT; PHOSPHORYLCHOLINE-CONTAINING GLYCOPROTEIN; COLLAGEN-INDUCED ARTHRITIS; TRICHURIS-SUIS THERAPY; NONOBESE DIABETIC MICE; SCHISTOSOMA-MANSONI; MULTIPLE-SCLEROSIS; HYGIENE HYPOTHESIS; T-CELLS; DENDRITIC CELLS;
D O I
10.1016/j.autrev.2014.10.004
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The incidence of autoimmune diseases has risen throughout the last half a century, mostly in the industrialized world. Helminths and their derivatives were found to have a protective role in autoimmunity and inflammatory conditions, as they manipulate the immune network, attenuating the host's cellular and humoral responses. Indeed, various helminth species used in several human and animal models were shown to limit inflammatory activity in a variety of diseases including inflammatory bowel disease, multiple sclerosis, type 1 diabetes, and rheumatoid arthritis. Our review will focus on the main mechanisms by which helminths and their secreted molecules modulate the host's immune system. The main pathways induce a shift from Th1 to Th2 phenotype, accelerate T regulatory and B regulatory phenotypes, and attenuate the levels of the inflammatory cytokines, leading to a tolerable scenario. (C) 2014 Elsevier B.V. All rights reserved.
引用
收藏
页码:98 / 104
页数:7
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