| First Author | Dianda L | Year | 1997 |
| Journal | Am J Pathol | Volume | 150 |
| Issue | 1 | Pages | 91-7 |
| PubMed ID | 9006326 | Mgi Jnum | J:37699 |
| Mgi Id | MGI:85091 | Citation | Dianda L, et al. (1997) T cell receptor-alpha beta-deficient mice fail to develop colitis in the absence of a microbial environment. Am J Pathol 150(1):91-7 |
| abstractText | 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 hare yet to be identified. |
