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JCI table of contents: Nov. 8, 2007
Date:11/8/2007

or these contradictory reports by demonstrating that the inflammatory milieu is a critical factor in determining the importance of TNF-alpha to the T cell response.

Mice lacking either TNF-alpha or one of its receptors (TNFR1 and TNFR2) were found to mount strong antiviral CD8+ T cell responses targeting the lymphocytic choriomeningitis virus glycoprotein (GP). By contrast, CD8+ T cell responses targeting tumors engineered to express the same GP protein were abrogated in TNF-alphadeficient mice. Further analysis revealed that TNF-alpha was required for several steps of the antitumor CD8+ T cell response. These data led the authors to suggest that cancer might be a long-term complication of prolonged blockade of TNF-alpha, such as occurs in patients taking TNF-alpha antagonists.

TITLE: TNF-alpha is critical for antitumor but not antiviral T cell immunity in mice

AUTHOR CONTACT:
Pamela S. Ohashi
Ontario Cancer Institute, Toronto, Ontario, Canada.
Phone: (416) 946-2357; Fax: (416) 946-2086; E-mail: pohashi@uhnres.utoronto.ca.

View the PDF of this article at: https://www.the-jci.org/article.php?id=32567


PULMONARY: Making mice breathe easy: a role for IL-1 in lung damage

Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal lung disease of unknown cause for which there is no effective treatment. Sequential episodes of acute lung injury that are followed by the formation of scar tissue (a process known as fibrosis) characterize IPF and ultimately lead to respiratory failure. In a new study, Isabelle Couillin and colleagues from the University of Orleans, France, have now identified some of the molecular mechanisms underlying inflammation-induced fibrosis in a mouse model of IPF.

When exposed to bleomycin, mice lacking either IL-1R1 or MyD88, which is crucial for the s
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Contact: Karen Honey
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Journal of Clinical Investigation
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