International Immunology, Vol. 13, No. 12, 1561-1570,
December 2001
© 2001 Japanese Society for Immunology
CD4 T cells monospecific to ovalbumin produced by Escherichia coli can induce colitis upon transfer to BALB/c and SCID mice
1 Divisions of Clinical Bio-regulatory Science, and
2 Gastroenterology and Hepatology, Graduate School of Medicine, Kyoto University, 54 Shogo-in, Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan
3 Division of Host Defense Mechanism, Department of Immunology, Tokai University School of Medicine, Kanagawa 259–1193, Japan
Correspondence to: Y. Wakatsuki
Although some animal models suggest an involvement of CD4 T cells reactive to luminal microrbial antigen(s) for the pathogenesis of inflammatory bowel diseases (IBD), direct linkage between microflora-driven clonal expansion of CD4 T cells and the development of colitis has not been well studied. Here, BALB/c and SCID mice were given CD4 T cells purified from Rag-2-/- mice crossed to transgenic mice expressing TCR specific to ovalbumin (OVA) then administered with antibiotic-resistant Escherichia coli producing OVA (ECOVA) or LacZ (ECLacZ) via the rectum. The ECOVA-inoculated BALB/c and SCID mice developed a subacute colitis with microscopic features of distortion of crypt architecture, loss of goblet cells, and focal infiltration by mononuclear cells in the lamina propria (LP) and submucosa. Expanding OVA-specific CD4 T cells were detected in colonic follicles of mice with ECOVA. Early in colitis, OVA-specific CD4 T cells producing IFN-
predominate in the LP of the colon, which was followed by an emergence of OVA-specific CD4 T cells producing IL-4 and IL-10 at a later time point. Co-transfer of an IL-10-secreting OVA-specific CD4 T cell line prevented colitis. Thus, an expansion of CD4 T cells monospecific to OVA, an antigen non-cross-reactive to colonic tissue, can mediate both induction and inhibition of the colitis which was associated with hyperplasia of lymph follicles.
Keywords: animal model, bacterial flora, Crohn's disease, cytokines, inflammatory bowel disease, mucosa, transgenic mice, ulcerative colitis
Transmitting editor: T. Kurosaki
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