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InterIeukin-23/Th17 Pathways and Inflammatory Bowel Disease

期刊

INFLAMMATORY BOWEL DISEASES
卷 15, 期 7, 页码 1090-1100

出版社

OXFORD UNIV PRESS INC
DOI: 10.1002/ibd.20894

关键词

inflammatory bowel disease; inflammation; autoimmunity; IL-23; Th17 cells

资金

  1. NCRR NIH HHS [UL1 RR024139] Funding Source: Medline
  2. NIDDK NIH HHS [U01 DK62429, U01 DK062422, DK P30-34989, R01DK077905, R01DK072373] Funding Source: Medline

向作者/读者索取更多资源

The IL-23/Th17pathway has recently been identified to play a critical role in a number of chronic inflammatory diseases including inflammatory bowel disease (IBD). The identification in IBD patients of associations in IL23R and regions that include other genes in the IL-23/Th17pathway has highlighted the importance of proper IL-23/Th17pathway regulation in intestinal immune homeostasis. IL-23 plays a role in CD4+ Th17 lineage cells, characterized by IL-17 secretion and the expression of the transcription factor retinoic acid-related orphan receptor (ROR)gamma tau, and in other immune and nonimmune cells. The balance between effector T cell Subsets, Such as Th17cells, and CD4+ T regulatory subsets is finely regulated: dysregulation of this balance can lead to inflammation and autoimmunity. As such, the IL-23/Th17pathway contributes to immune responses that play a role in defenses to microbial infection, as well as in the intestinal inflammation observed in both animal models of colitis and human IBD. (Inflamm Bowel Dis 2009:15:1090-1100)

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