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Blood, 1 December 2005, Vol. 106, No. 12, pp. 4009-4015. Prepublished online as a Blood First Edition Paper on August 16, 2005; DOI 10.1182/blood-2005-06-2339. This Article Full Text (PDF) All Versions of this Article: 2005-06-2339v1 106/12/4009    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Dutt, S. Articles by Strober, S. Search for Related Content PubMed PubMed Citation Articles by Dutt, S. Articles by Strober, S. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted June 13, 2005 Accepted July 31, 2005 L-Selectin and 7 integrin on donor CD4 T cells are required for the early migration to host mesenteric lymph nodes and acute colitis of graft versus host disease Suparna Dutt, Joerg Ermann, Diane Tseng, Yin Ping Liu, Tracy I George, C G Fathman, and Samuel Strober* Department of Medicine, Stanford University School of Medicine, Sanford University, Stanford, CA, USA Department of Pathology, Stanford University School of Medicine, Sanford University, Stanford, CA, USA * Corresponding author; email: sstrober{at}stanford.edu. The homing receptors L-Selectin and 4 7 integrin facilitate entry of T cells into the gut associated organized lymphoid tissues such as the mesenteric lymph nodes and Peyer's patches. We studied the impact of inactivation of genes encoding these receptors on the ability of purified donor CD4+ T cells to induce acute lethal graft versus host disease (GVHD) associated with severe colitis in irradiated MHC- mismatched mice. Whereas lack of expression of a single receptor had no significant impact on the severity of colitis and GVHD, the lack of expression of both receptors markedly ameliorated colitis and early deaths observed with wild-type (WT) T cells. The changes in colitis and GVHD was reflected in a marked reduction in the early accumulation of donor T cells in the mesenteric lymph nodes, and subsequently in the colon. The purified WT donor CD4+ T cells did not accumulate early in the Peyer's patches and failed to induce acute injury to the small intestine. In conclusion, the combination of CD62L and 7 integrin are required to induce acute colitis and facilitate entry of CD4+ donor T cells in the mesenteric nodes associated with lethal GVHD in allogeneic hosts. 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