COMMENTARY
See article on page 477
Pathogenesis of inflammatory bowel disease: transcription factors in the spotlight
| The first 150 words of the full text of this article appear below. |
Dysregulated cytokine production by mucosal lymphocytes and
macrophages has been implicated in the pathogenesis of both Crohn's disease and ulcerative colitis, the two major forms of human
inflammatory bowel disease (IBD).1 Over the past few
years, various murine models of chronic intestinal inflammation
resembling IBD have been discovered which have provided important clues
as to the nature of this dysregulation and to its possible treatment
with cytokines.2 Thus, in studies of several of the models
most closely resembling Crohn's disease it has been shown that
production of large amounts of Th1-type cytokines
for example,
interferon
, by T cells is a major and essential feature of the
inflammation.2 In addition, it has been shown that this
disease causing Th1 cytokine response can be counteracted by induction
of a suppressor response involving the generation of T cells producing
Th2-type cytokines or transforming growth factor
.3
Finally, it has been shown that
Relevant Article
-
Activation of nuclear factor
B in inflammatory bowel disease
- S Schreiber, S Nikolaus, and J Hampe
Gut 1998 42: 477-484.[Abstract] [Full Text] [PDF]
This article has been cited by other articles:
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Thiele, K, Bierhaus, A, Autschbach, F, Hofmann, M, Stremmel, W, Thiele, H, Ziegler, R, Nawroth, P P
(1999). Cell specific effects of glucocorticoid treatment on the NF-kappa Bp65/Ikappa Balpha system in patients with Crohn's disease. Gut
45: 693-704
[Abstract] [Full Text]
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