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J. Exp. Med.,
Volume 189, Number 8, April 19, 1999 1169-1180
By

¶
From the * Immunobiology Vaccine Center, Department of Microbiology and To investigate the potential involvement of T helper (Th)2-type responses in murine models of
intestinal inflammation, we used trinitrobenzene sulfonic acid (TNBS)-hapten to induce inflammatory bowel disease in situations where Th1-type responses with interferon (IFN)-
Department of Oral
Biology, The University of Alabama at Birmingham, Birmingham, Alabama 35294; § Biogen
Incorporated, Cambridge, Massachusetts 02142; and the ¶ Department of Mucosal Immunology,
Research Institute for Microbial Diseases, Osaka University, Suita, Osaka 565, Japan
synthesis are either diminished or do not occur. Intracolonic administration of TNBS to either
normal (IFN-
+/+) or Th1-deficient IFN-
knockout (IFN-
/
) BALB/c mice resulted in
significant colitis. In IFN-
/
mice, crypt inflammation was more severe than in IFN-
+/+
mice and was accompanied by hypertrophy of colonic patches with a lymphoepithelium containing M cells and distinct B and T cell zones resembling Peyer's patches. Hapten-specific, colonic patch T cells from both mouse groups exhibited a Th2 phenotype with interleukin (IL)-4
and IL-5 production. TNBS colitis in normal mice treated with anti-IL-4 antibodies or in IL-4
/
mice was less severe than in either IFN-
+/+ or IFN-
/
mice. Our findings now show that
the Th2-type responses in TNBS colitis are associated with colonic patch enlargement and inflammation of the mucosal layer and may represent a model for ulcerative colitis.
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