The University of Southampton
University of Southampton Institutional Repository

Recent developments in the immunology of inflammatory bowel disease

Recent developments in the immunology of inflammatory bowel disease
Recent developments in the immunology of inflammatory bowel disease
Crohn's disease and ulcerative colitis are caused by excessive immune reactivity in the gut wall. Analysis of the type of immune responses ongoing in diseased gut has revealed important features which suggest that these conditions are different. In Crohn's disease tissue there is considerable evidence for an ongoing T helper cell type 1 response, with excess interleukin-12, interferon-gamma and TNF-alpha. There is circumstantial evidence in patients that this response is directed against the normal bacterial flora and definitive evidence in mouse models that T cell responses to the flora cause gut disease. In ulcerative colitis, the role of tissue damaging T cell responses in the gut mucosa is much less clear and there is more evidence that the lesion is owing to antibody-mediated hypersensitivity. Although different types of immune reactions initiate tissue injury in both Crohn's disease and ulcerative colitis, the downstream events which actually damage the tissue are the same in each condition. Elevated cytokine concentrations in the mucosa lead to the production of excess matrix degrading enzymes by gut fibroblasts, loss of mucosal integrity and ulceration. The same process also leads to an increased production of epithelial growth factors such as KGF Keratinocyte Growth Factor by gut fibroblasts and produces the crypt cell hyperplasia characteristic of all gut inflammatory conditions.
0300-9475
2-9
MacDonald, T.T.
171334aa-638a-42b0-99f6-e860e2f0ca45
Monteleone, G.
bd762d44-920a-4c7d-afb3-b7a123399e73
Pender, S.L.
62528b03-ec42-41bb-80fe-48454c2c5242
MacDonald, T.T.
171334aa-638a-42b0-99f6-e860e2f0ca45
Monteleone, G.
bd762d44-920a-4c7d-afb3-b7a123399e73
Pender, S.L.
62528b03-ec42-41bb-80fe-48454c2c5242

MacDonald, T.T., Monteleone, G. and Pender, S.L. (2000) Recent developments in the immunology of inflammatory bowel disease. Scandinavian Journal of Immunology, 51 (1), 2-9. (doi:10.1046/j.1365-3083.2000.00658.x).

Record type: Article

Abstract

Crohn's disease and ulcerative colitis are caused by excessive immune reactivity in the gut wall. Analysis of the type of immune responses ongoing in diseased gut has revealed important features which suggest that these conditions are different. In Crohn's disease tissue there is considerable evidence for an ongoing T helper cell type 1 response, with excess interleukin-12, interferon-gamma and TNF-alpha. There is circumstantial evidence in patients that this response is directed against the normal bacterial flora and definitive evidence in mouse models that T cell responses to the flora cause gut disease. In ulcerative colitis, the role of tissue damaging T cell responses in the gut mucosa is much less clear and there is more evidence that the lesion is owing to antibody-mediated hypersensitivity. Although different types of immune reactions initiate tissue injury in both Crohn's disease and ulcerative colitis, the downstream events which actually damage the tissue are the same in each condition. Elevated cytokine concentrations in the mucosa lead to the production of excess matrix degrading enzymes by gut fibroblasts, loss of mucosal integrity and ulceration. The same process also leads to an increased production of epithelial growth factors such as KGF Keratinocyte Growth Factor by gut fibroblasts and produces the crypt cell hyperplasia characteristic of all gut inflammatory conditions.

This record has no associated files available for download.

More information

Published date: January 2000

Identifiers

Local EPrints ID: 73604
URI: http://eprints.soton.ac.uk/id/eprint/73604
ISSN: 0300-9475
PURE UUID: d87feb19-1d32-4c9c-a2e7-df37725cf812
ORCID for S.L. Pender: ORCID iD orcid.org/0000-0001-6332-0333

Catalogue record

Date deposited: 10 Mar 2010
Last modified: 14 Mar 2024 02:45

Export record

Altmetrics

Contributors

Author: T.T. MacDonald
Author: G. Monteleone
Author: S.L. Pender ORCID iD

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton: eprints@soton.ac.uk

ePrints Soton supports OAI 2.0 with a base URL of http://eprints.soton.ac.uk/cgi/oai2

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.

×