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Interleukin-10-deficient mice develop chronic enterocolitis.

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Affiliations

  • 1. Institute for Genetics, University of Cologne, Federal Republic of Germany.
      Authors
    • Kühn R 1
    (1 author)

ORCIDs linked to this article

Cell, 01 Oct 1993, 75(2):263-274
https://doi.org/10.1016/0092-8674(93)80068-p PMID: 8402911 

A comment on this article appears in "Chronic intestinal inflammation: an unexpected outcome in cytokine or T cell receptor mutant mice." Cell. 1993 Oct 22;75(2):203-5.

Abstract 

Interleukin-10 (IL-10) affects the growth and differentiation of many hemopoietic cells in vitro; in particular, it is a potent suppressor of macrophage and T cell functions. In IL-10-deficient mice, generated by gene targeting, lymphocyte development and antibody responses are normal, but most animals are growth retarded and anemic and suffer from chronic enterocolitis. Alterations in intestine include extensive mucosal hyperplasia, inflammatory reactions, and aberrant expression of major histocompatibility complex class II molecules on epithelia. In contrast, mutants kept under specific pathogen-free conditions develop only a local inflammation limited to the proximal colon. These results indicate that the bowel inflammation in the mutants originates from uncontrolled immune responses stimulated by enteric antigens and that IL-10 is an essential immunoregulator in the intestinal tract.

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