Chronic colitis in IL-10-/- mice: insufficient counter regulation of a Th1 response.

Abstract:

:IL-10-deficient (IL-10-/-) mice, generated by a gene-targeted mutation, develop abnormal immune responses as a result of uncontrolled interactions between antigen presenting cells and lymphocytes. The studies reviewed herein have focused on the enterocolitis that spontaneously develops in IL-10-/- mice. Not unexpectedly, heightened production of proinflammatory mediators accompanied pathologic changes in the gastrointestinal tract of young mutants. In a series of studies, the proinflammatory mediators responsible for initiating the pathogenic response were distinguished from those that were elicited as a consequence of persistent inflammation. We have also investigated the possibility that different mediators are involved in the inductive versus the maintenance phase of disease. The findings of these mechanistic studies as they relate to our understanding of progressive inflammatory disease and the role of IL-10 in controlling the acute and chronic stages are discussed.

journal_name

Int Rev Immunol

authors

Davidson NJ,Fort MM,Müller W,Leach MW,Rennick DM

doi

10.3109/08830180009048392

subject

Has Abstract

pub_date

2000-01-01 00:00:00

pages

91-121

issue

1

eissn

0883-0185

issn

1563-5244

journal_volume

19

pub_type

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