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The Journal of Immunology, 1999, 162: 4975-4982.
Copyright © 1999 by The American Association of Immunologists

Administration of mAb Against {alpha}Eß7 Prevents and Ameliorates Immunization-Induced Colitis in IL-2-/- Mice

Björn R. Lúdvíksson1,*, Warren Strober*, Ryuta Nishikomori*, Syed K. Hasan* and Rolf O. Ehrhardt*,{dagger}

* Mucosal Immunity Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, and {dagger} Protein Design Laboratories, Inc., Mountain View, CA 94043

We previously demonstrated that 2,4,6-trinitrophenol (TNP)-OVA immunization leads to a transmural colitis in the IL-2-/- mouse that is caused by IL-12-driven CD4+ Th1 T cells and resembles human Crohn’s disease. The integrin {alpha}Eß7 is highly expressed on colonic intraepithelial lymphocytes and has been suggested to function as a homing or retention molecule for intraepithelial lymphocytes. To evaluate the role of {alpha}Eß7 in colitis, we administered a mAb against {alpha}Eß7 to IL-2-/- mice that were immunized at the same time with TNP-OVA in CFA. To our surprise, this treatment resulted in a significantly reduced colitis severity score, 0–2 vs 3–4, that was associated with a significant reduction in CD4+ lamina propria lymphocyte subpopulation (p < 0.01). In contrast, the total number of splenic CD4+ T cells of treated animals was significantly elevated compared with that of untreated animals (3.2 ± 0.6 x 107 vs 1.2 ± 0.2 x 107; p < 0.05). Similarly, functional studies revealed that IFN-{gamma} production by lamina propria lymphocytes isolated from IL-2-/- TNP-OVA-immunized mice treated with anti-{alpha}Eß7 was significantly lower than in untreated IL-2-/- TNP-OVA-immunized mice. In contrast, IFN-{gamma} production by splenic cells isolated from treated IL-2-/- TNP-OVA-immunized mice was significantly higher than in untreated mice. Finally, TNP-OVA-immunized IL-2-/- mice that were treated after the colitis had been established also showed a significant decrease in mucosal inflammation after {alpha}Eß7 mAb administration. Thus, the above findings demonstrate that the onset and maintenance of inflammatory bowel disease depends on the colonic localization of lamina propria CD4+ lymphocytes expressing {alpha}Eß7.




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