The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
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Published 7 January 2002. doi:10.1084/jem.2001889
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© Rockefeller University Press, 0022-1007/2002/1/71/ $5.00
The Journal of Experimental Medicine, Volume 195, Number 1, January 7, 2002 71-84

Original Article

T Helper 1 and T Helper 2 Cells Are Pathogenic in an Antigen-specific Model of Colitis

Nuzhat Iqbal2, James R. Oliver1, Frederic H. Wagner1, Audrey S. Lazenby1, Charles O. Elson2 and Casey T. Weaver1

1 Department of Pathology, University of Alabama at Birmingham, Birmingham, AL 35233
2 Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35233

Address correspondence to Casey T. Weaver, Dept. of Pathology, University of Alabama at Birmingham, 845 19th St. South, BBRB 870, Birmingham, AL 35233-7331. Phone: 205-975-5537; Fax: 205-975-8310; E-mail: weaver{at}path.uab.edu

Dysregulated T cell responses to enteric bacteria have been implicated as a common mechanism underlying pathogenesis in rodent models of colitis. However, the bacterial species and T cell specificities that induce disease have been poorly defined. We have developed a model system in which target antigen, bacterial host, and corresponding T cell specificity are defined. OVA-specific T cells from DO11.RAG-2-/- TCR transgenic mice were transferred into RAG-2-/- recipients whose intestinal tracts were colonized with OVA-expressing or control Escherichia coli. Transfer of antigen-naive DO11.RAG-2-/- T cells into recipients colonized with OVA-E. coli resulted in enhanced intestinal recruitment and cell cycling of OVA-specific T cells; however, there was no development of disease. In contrast, transfer of polarized T helper (Th) 1 and Th2 populations resulted in severe wasting and colitis in recipients colonized with OVA-expressing but not control E. coli. The histopathologic features of disease induced by Th1 and Th2 transfers were distinct, but disease severity was comparable. Induction of disease by both Th1 and Th2 transfers was dependent on bacterially associated OVA. These results establish that a single bacterially associated antigen can drive the progression of colitis mediated by both Th1 and Th2 cells and provide a new model for understanding the immunoregulatory interactions between T cells responsive to gut floral antigens.

Key Words: inflammatory bowel disease • E. coli • CD4 • cytokines • TCR transgenic


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