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Curr Opin Gastroenterol. 2008 Jul;24(4):455-61. doi: 10.1097/MOG.0b013e328304d60d.

Adaptive immunity in inflammatory bowel disease: state of the art.

Author information

1
Division of Gastroenterology, Department of Medicine, Innsbruck Medical University, Innsbruck, Austria. arthur.kaser@i-med.ac.at

Abstract

PURPOSE OF REVIEW:

Adaptive immune mechanisms are inherently involved in the pathogenesis of inflammatory bowel disease. This review summarizes the main discoveries made in 2007 within this field.

RECENT FINDINGS:

CD4 T cells secreting interleukin-17 (T helper type 17) cells have emerged as a key effector population driving colitis in animal models previously associated with exaggerated T helper type 1 responses. With regard to T-regulatory cells, a novel suppressive cytokine (interleukin-35) and induction of apoptosis as a means to exert suppression have been identified. The importance of specific chemokine receptors and integrins in effector and T-regulatory cell function in colitis has been recognized.

SUMMARY:

An improved understanding of adaptive immune mechanisms, on which manifold genetic and environmental traits might converge, and which ultimately mediate intestinal inflammation in inflammatory bowel disease, holds promise for novel effective therapeutic intervention.

PMID:
18622159
DOI:
10.1097/MOG.0b013e328304d60d
[Indexed for MEDLINE]
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