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(American Journal of Pathology. 2004;165:1257-1268.)
© 2004 American Society for Investigative Pathology

CD4+CD45RBHi Interleukin-4 Defective T Cells Elicit Antral Gastritis and Duodenitis

Taeko Dohi*{dagger}, Kohtaro Fujihashi{ddagger}, Toshiya Koga{ddagger}, Yuri Etani{ddagger}, Naoto Yoshino{ddagger}, Yuki I. Kawamura* and Jerry R. McGhee{dagger}

From the Department of Gastroenterology,* Research Institute, International Medical Center of Japan, Tokyo, Japan; the Departments of Oral Biology,{ddagger} School of Dentistry, and The Immunobiology Vaccine Center, Department of Microbiology,{dagger} The University of Alabama at Birmingham, Birmingham, Alabama

We have analyzed the gastrointestinal inflammation which develops following adoptive transfer of IL-4 gene knockout (IL-4–/–) CD4+CD45RBHi (RBHi) T cells to severe combined immunodeficient (SCID) or to T cell-deficient, T cell receptor ß and {delta} double knockout (TCR–/–) mice. Transfer of IL-4–/– RBHi T cells induced a similar type of colitis to that seen in SCID or TCR–/– recipients of wild-type (wt) RBHi T cells as reported previously. Interestingly, transfer of both wt and IL-4–/– RBHi T cells to TCR–/– but not to SCID mice induced inflammation in the gastric mucosa. Notably, TCR–/– recipients of IL-4–/– RBHi T cells developed a more severe gastritis with erosion, apoptosis of the antral epithelium, and massive infiltration of macrophages. This gastritis was partially dependent on the indigenous microflora. Recipients of both wt and IL-4–/– RBHi T cells developed duodenitis with multinuclear giant cells, expansion of mucosal macrophages, and dendritic cells. Full B cell responses were reconstituted in TCR–/– recipients of RBHi T cells; however, anti-gastric autoantibodies were not detected. We have now developed and characterized a novel model of chronic gastroduodenitis in mice, which will help in our understanding of the mechanisms involved in chronic inflammation in the upper gastrointestinal tract of humans.




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