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Roles of galectins in inflammatory bowel disease

Roles of galectins in inflammatory bowel disease

作     者:Akira Hokama Emiko Mizoguchi Atsushi Mizoguchi 

作者机构:Department of Medicine and Therapeutics (First Department of Internal Medicine) Control and Prevention of Infectious Disease Faculty of Medicine University of the RyukyusOkinawa 903-0215 Japan Gastrointestinal Unit Department of Medicine Massachusetts General Hospital Harvard Medical SchoolBoston MA 02114 United States Center for the Study of Inflammatory Bowel Disease Massachusetts General Hospital Harvard Medical School Boston MA 02114 United States Experimental Pathology Unit Department of Pathology Massachusetts General Hospital Harvard Medical SchoolBoston MA 02114 United States 

出 版 物:《World Journal of Gastroenterology》 (世界胃肠病学杂志(英文版))

年 卷 期:2008年第14卷第33期

页      面:5133-5137页

核心收录:

学科分类:1002[医学-临床医学] 100201[医学-内科学(含:心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

基  金:National Institute of Health Grants, No. DK64289 and DK74454 IBD grants from the Eli and Edythe L. Broad Medical Foundation National Institute of Health grant, DK64351 IBD grants from the Eli and Edythe L. Broad Medical Foundation 

主  题:Galectin Inflammatory bowel disease Crohn's disease Ulcerative colitis Pathogenesis Apoptosis Glycosylation 

摘      要:Protein/carbohydrate interactions through specific protein families termed lectin control essential biological processes. Galectins, a family of animal lectins defined by shared amino acid sequence with affinity for β-galactosides, appear to be functionally polyvalent in a wide range of biological activity. Recent studies have identified immunoregulatory roles of galectins in intestinal inflammatory disorders. Galectin-1 and galectin -2 contribute to the suppression of intestinal inflammation by the induction of apoptosis of activated T cells, whereas galectin-4 is involved in the exacerbation of this inflammation by specifically stimulating intestinal CD4+ T cells to produce IL-6. We review how different members of the galectins provide inhibitory or stimulatory signals to control intestinal immune response under intestinal inflammation.

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