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JCI online early table of contents: Jan. 10 2008
Date:1/10/2008

cted Th2 effector cells were detectable, whereas chemokines that attracted Th1 effector cells were not detectable. Consistent with this, only cytokines produced by Th2 cells were found that the site of L. major infection. Further analysis indicated that L. major induced the production of the chemokine CCL7, which attracts Th2 effector cells. The authors therefore concluded that pathogens can modify the chemokine profile at the site of dermal infection and thereby modulate the type of immune effector T cell that is recruited.

TITLE: Pathogen-imposed skewing of mouse chemokine and cytokine expression at the infected tissue site

AUTHOR CONTACT:
Deborah J. Fowell
University of Rochester, Rochester, New York, USA.
Phone: (585) 273-3680; Fax: (585) 273-2452; E-mail: deborah_fowell@urmc.rochester.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=33174


GASTROENTEROLOGY: TLRs given the NOD: the protein NOD2 negatively regulates TLR signaling

A substantial subset of individuals with the inflammatory bowel disease Crohn disease (CD) have mutations in their CARD15 gene, which is the gene that allows individuals to make the protein NOD2. The mechanisms underlying the link between CARD15 mutations and CD have not been clearly determined. One possibility, however, is that the genetic mutations lead to the generation of mutant forms of NOD2 that are unable to negatively regulate signaling by a receptor for bacterial products known as TLR2; the dysregulated TLR2 signaling is then proposed to activate an excessive inflammatory response in the gut. New data generated in mice has led Warren Strober and colleagues at the National Institutes of Health, Bethesda, to extend this hypothesis such that they have proposed that NOD2 negatively regulates signaling by multiple receptors
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Contact: Karen Honey
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Journal of Clinical Investigation
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