期刊
JOURNAL OF GASTROENTEROLOGY
卷 43, 期 1, 页码 1-17出版社
SPRINGER JAPAN KK
DOI: 10.1007/s00535-007-2111-3
关键词
antigen sampling; autophagy; IBD; Breg; mucin; NOD2; Th17; TLRs
资金
- NIDDK NIH HHS [DK74454, DK64351, DK64289, DK43351] Funding Source: Medline
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R03DK074454, R01DK064351, P30DK043351, K08DK064289] Funding Source: NIH RePORTER
Accumulating data from animal models indicate that inflammatory bowel disease (IBD) is mediated by a much more complicated mechanism than previously predicted. For example, the role of an individual molecule in the pathogenesis of IBD distinctly differs depending on several factors, including the fundamental mechanism of induction of the disease, the target cell type, the phase of disease, and the environment. Therefore, it has been difficult in the past to fully explain the complicated mechanism. Novel concepts have recently been proposed to further explain the complicated mechanism of IBD. In this review, we introduce past, current, and possible future concepts for IBD models regarding T helper (Th) 1, Th2, and Th17, antigen sampling and presentation, regulatory cell networks, NOD2, Toll-like receptors, bacteria/epithelia interaction, stem cells, autophagy, microRNAs, and glycoimmunology, and we also discuss the relevance of these new concepts, developed at the bench (in animal models), to the bedside.
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