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Proc Natl Acad Sci U S A. 2001 Nov 6;98(23):13306-11. Epub 2001 Oct 30.

Enterocolitis induced by autoimmune targeting of enteric glial cells: a possible mechanism in Crohn's disease?

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  • 1Institut National de la Santé et de la Recherche Médicale U546 and Immunology Laboratory, Pitié-Salpêtrière Hospital, Paris 75013, France.

Abstract

Early pathological manifestations of Crohn's disease (CD) include vascular disruption, T cell infiltration of nerve plexi, neuronal degeneration, and induction of T helper 1 cytokine responses. This study demonstrates that disruption of the enteric glial cell network in CD patients represents another early pathological feature that may be modeled after CD8(+) T cell-mediated autoimmune targeting of enteric glia in double transgenic mice. Mice expressing a viral neoself antigen in astrocytes and enteric glia were crossed with specific T cell receptor transgenic mice, resulting in apoptotic depletion of enteric glia to levels comparable in CD patients. Intestinal and mesenteric T cell infiltration, vasculitis, T helper 1 cytokine production, and fulminant bowel inflammation were characteristic hallmarks of disease progression. Immune-mediated damage to enteric glia therefore may participate in the initiation and/or the progression of human inflammatory bowel disease.

PMID:
11687633
[PubMed - indexed for MEDLINE]
PMCID:
PMC60866
Free PMC Article
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