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The Journal of Immunology, 1999, 162: 1884-1888.
Copyright © 1999 by The American Association of Immunologists

CUTTING EDGE

Cutting Edge: Chronic Intestinal Inflammation in STAT-4 Transgenic Mice: Characterization of Disease and Adoptive Transfer by TNF- Plus IFN-{gamma}-Producing CD4+ T Cells That Respond to Bacterial Antigens1

Stefan Wirtz*, Susetta Finotto*, Stephan Kanzler*, Ansgar W. Lohse*, Manfred Blessing*, Hans A. Lehr{dagger}, Peter R. Galle* and Markus F. Neurath2,*

* Laboratory of Immunology, I. Medical Clinic, University of Mainz, Mainz, Germany; and {dagger} Institute of Pathology, University of Mainz, Mainz, Germany

We generated transgenic mice for STAT-4, a regulatory protein specifically associated with IL-12 signaling, under the control of a CMV promoter. These mice expressed strikingly increased nuclear STAT-4 levels in lamina propria CD4+ T lymphocytes upon systemic administration of dinitrophenyl-keyhole limpet hemocyanin and developed chronic transmural colitis characterized by infiltrates of mainly CD4+ T lymphocytes. The latter cells produced predominantly TNF and IFN-{gamma} but not IL-4 upon activation with {alpha}CD3/CD28 or autologous bacterial Ags, consistent with a Th1-type cell response. Furthermore, chronic colitis in STAT-4 transgenic mice could be adoptively transferred to SCID mice by colonic and splenic CD4+ T cells that were activated with Ags from autologous bacterial flora. These data establish a critical molecular signaling pathway involving STAT-4 for the pathogenesis of chronic intestinal inflammation, and targeting of this pathway may be relevant for the treatment of colitis in humans.




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