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JCI table of contents: Oct. 2, 2006

ci.org/article.php?id=29021">https://www.the-jci.org/article.php?id=29021

ACCOMPANYING COMMENTARY
TITLE: Pili prove pertinent to enterococcal endocarditis

AUTHOR CONTACT:
Olaf Schneewind
University of Chicago, Chicago, Illinois, USA.
Phone: (773) 834-9060; Fax: (773) 834-8150; E-mail: oschnee@bsd.uchicago.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=30088


ONCOLOGY: Anti-tumor immune responses bring about their own demise

In the early stages of cancer an individual's immune system mounts an anti-tumor response to try and rid the body of the tumor. However, this immune response becomes blunted with time and the tumor is able to grow unimpeded. Understanding why the immune response becomes ineffective is a major goal of many researchers looking for ways to treat individuals with cancer. Now, in a mouse study appearing in the October issue of the Journal of Clinical Investigation, researchers from the Instituto Oncologico Veneto, Italy, have identified one pathway by which tumors suppress the anti-tumor response, providing new avenues of research for the development of anti-cancer drugs.

Previous studies have shown that tumors release soluble factors that recruit a population of cells known as myeloid suppressor cells (MSCs) because of their ability to suppress an immune response. Vincenzo Bronte and colleagues have now shown that MSCs marked by their expression of a protein known as IL-4R-alpha produce two soluble factors (IFN-gamma and IL-13) that are required for MSC suppression of the immune response. Ironically, IL-4R-alphaexpressing MSCs were activated to produce these soluble factors by the anti-tumor immune response going on at their time of recruitment to the tumor. This study describes one pathway by which the anti-tumor immune res
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Contact: Karen Honey
press_releases@the-jci.org
212-342-4159
Journal of Clinical Investigation
2-Oct-2006


Page: 1 2 3 4 5 6 7 8

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