T cell receptor-alpha beta-deficient mice fail to develop colitis in the absence of a microbial environment.
T cell receptor-alpha beta-deficient mice fail to develop colitis in the absence of a microbial environment.
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发表时间：
1997
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通讯作者：
L. Dianda;A. Hanby;N. Wright;A. Sebestény;A. Hayday;M. Owen
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作者：
L. Dianda;A. Hanby;N. Wright;A. Sebestény;A. Hayday;M. Owen
细胞因子或T细胞受体(TCR)基因零突变的小鼠会发生肠道炎症。在白介素2-/-和白介素10-/-小鼠的情况下，已经证明正常的肠道细菌群可以引起肠道病理。TCR-α-/-小鼠不仅会患上结肠炎，还会对自身抗原产生强烈的抗体反应，例如双链DNA。因此，重要的是要确定肠道炎症是自发发生的，还是由管腔抗原引起的。为了解决这个问题，我们获得了一个无菌的TCR-α-/-小鼠群体，并与保持在常规无特定病原体条件下的TCR-α-/-小鼠进行了比较。虽然无特定病原体的动物发生结肠炎的外显率很高，但没有证据表明无细菌动物的肠道病理。此外，在由植物乳杆菌、粪链球菌、粪链球菌和/或大肠杆菌组成的有限细菌群定居的TCR-α/-小鼠中，没有发现肠道炎症。我们的结论是，TCR-α-/-小鼠的肠道炎症不是自发发生的，也不是由细菌本身的存在引起的，而是由通常存在于肠道菌群中的一种或一组尚未确定的特定生物体引起的。
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.