The Journal of Experimental Medicine
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Published online
doi:10.1084/jem.20071160
The Journal of Experimental Medicine, Vol. 205, No. 6, 1463-1476
The Rockefeller University Press, 0022-1007 $30.00
© Steinberg et al.
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ARTICLE

 A crucial role for HVEM and BTLA in preventing intestinal inflammation

Marcos W. Steinberg1, Olga Turovskaya1, Raziya B. Shaikh1, Gisen Kim1, Declan F. McCole3, Klaus Pfeffer4, Kenneth M. Murphy5, Carl F. Ware2, and Mitchell Kronenberg1

1 Division of Developmental Immunology and 2 Division of Molecular Immunology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037
3 Division of Gastroenterology, Department of Medicine, University of California San Diego, School of Medicine, La Jolla, CA 92093
4 Institute of Medical Microbiology, Heinrich-Heine-Universität Düsseldorf, D-40225 Düsseldorf, Germany
5 Department of Pathology and Center for Immunology, and Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, MO 63110

CORRESPONDENCE Mitchell Kronenberg: mitch{at}liai.org

The interaction between the tumor necrosis factor (TNF) family member LIGHT and the TNF family receptor herpes virus entry mediator (HVEM) co-stimulates T cells and promotes inflammation. However, HVEM also triggers inhibitory signals by acting as a ligand that binds to B and T lymphocyte attenuator (BTLA), an immunoglobulin super family member. The contribution of HVEM interacting with these two binding partners in inflammatory processes remains unknown. In this study, we investigated the role of HVEM in the development of colitis induced by the transfer of CD4+CD45RBhigh T cells into recombination activating gene (Rag)–/– mice. Although the absence of HVEM on the donor T cells led to a slight decrease in pathogenesis, surprisingly, the absence of HVEM in the Rag–/– recipients led to the opposite effect, a dramatic acceleration of intestinal inflammation. Furthermore, the critical role of HVEM in preventing colitis acceleration mainly involved HVEM expression by radioresistant cells in the Rag–/– recipients interacting with BTLA. Our experiments emphasize the antiinflammatory role of HVEM and the importance of HVEM expression by innate immune cells in preventing runaway inflammation in the intestine.

Abbreviations used: BTLA, B and T lymphocyte attenuator; DSS, dextran sodium sulfate; GVHD, graft versus host disease; H&E, hematoxylin and eosin; HVEM, herpes virus entry mediator; IBD, inflammatory bowel disease; IEC, intestinal epithelial cell; IEL, intestinal epithelial lymphocyte; LPL, lamina propria lymphocyte; MLN, mesenteric lymph node.

© 2008 Steinberg et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jgp.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).


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