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American Journal of Pathology, Vol 150, 91-97, Copyright © 1997 by American Society for Investigative Pathology

REGULAR ARTICLES

T cell receptor-alpha beta-deficient mice fail to develop colitis in the absence of a microbial environment

L Dianda, AM Hanby, NA Wright, A Sebesteny, AC Hayday and MJ Owen
Imperial Cancer Research Fund, London, United Kingdom.

Mice with null mutations in cytokine or T cell receptor (TCR) genes develop intestinal inflammation. In the case of interleukin-2-/- and interleukin-10-/- mice it has been demonstrated that normal intestinal bacterial flora can cause gut pathology. TCR-alpha-/- mice not only develop colitis but also produce a strong antibody response to self- antigens, such as double-stranded DNA. It is therefore important to establish whether the intestinal inflammation develops spontaneously or is induced by luminal antigens. To address this issue, a germ-free colony of TCR-alpha-/- mice was derived and compared with TCR-alpha-/- mice kept in conventional specific-pathogen-free conditions. Although specific-pathogen-free animals developed colitis with a high level of penetrance, there was no evidence of intestinal pathology in germ-free animals. Furthermore, intestinal inflammation was not seen in TCR-alpha- /- mice colonized with a limited bacterial flora consisting of Lactobacillus plantarum, Streptococcus faecalis, S. faecium, and/or Escherichia coli. We conclude that intestinal inflammation in TCR-alpha- /- mice does not occur spontaneously nor does it result from the presence of bacteria, per se, but rather it is initiated by a specific organism or group of organisms normally present in the gut flora that have yet to be identified.


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