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JCI table of contents: Sept. 4, 2007
Date:9/4/2007

te the sites to which they can home; for example, integrin alpha4beta7 directs T cells to the gut. Modulating integrin adhesiveness might therefore provide a way to alter T cell homing for the treatment of pathogenic gut inflammation.

Motomu Shimaoka and colleagues at the CBR Institute for Biomedical Research, Boston, genetically modified the ADMIDAS regulatory domain of the beta7 chain of the integrin alpha4beta7 such that integrin alpha4beta7 was persistently in its active state. T cells in these mice failed to migrate properly because the integrin alpha4beta7 was persistently bound to its ligand MAdCAM-1. These mice therefore had fewer T cells in their gut. Furthermore, T cells from these mice had a reduced capacity to induce colitis. As discussed in the accompanying commentary by Ivor Douglas and Themistocles Dassopoulos, this demonstration of the importance of the ADMIDAS domain in controlling integrin de-adhesion is crucial for the future design of small molecules for the treatment chronic inflammatory conditions such as colitis.

TITLE: Aberrant activation of integrin alpha4beta7 suppresses lymphocyte migration to the gut

AUTHOR CONTACT:

Motomu Shimaoka
CBR Institute for Biomedical Research, Boston, Massachusetts, USA.
Phone: (617) 278-3272; Fax: (617) 278-3232; E-mail: shimaoka@cbrinstitute.org.

View the PDF of this article at: https://www.the-jci.org/article.php?id=31570

ACCOMPANYING COMMENTARY

TITLE: Rheostat regulation of integrin-mediated leukocyte adhesion

AUTHOR CONTACT:

Ivor S. Douglas
University of Colorado at Denver and Health Sciences Center, Denver, Colorado, USA.
Phone: (303) 436-5905; Fax: (303) 436-7249; E-mail: idouglas@dhha.org.

View the PDF of this article at:

Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation
Source:Eurekalert

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