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 Blood, 13 August 2009, Vol. 114, No. 7, pp. 1344-1354.
Prepublished online as a Blood First Edition Paper on June 16, 2009; DOI 10.1182/blood-2008-12-196592.

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Submitted December 23, 2008
Accepted June 8, 2009

Interferon beta induces mature dendritic cell apoptosis through caspase-11 / caspase-3 activation

Jui-Hung Yen and Doina Ganea*

Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA, United States

* Corresponding author; email: doina.ganea{at}temple.edu.

Although IFN{beta} decreases relapse rate and disease activity in multiple sclerosis (MS), the mechanisms involved have not been elucidated. The present study is the first report on the apoptotic effect of IFN{beta} in mature, but not immature myeloid dendritic cells (DC). Both exogenous IFN{beta} added to DC matured through exposure to proinflammatory cytokines, and endogenous IFN{beta} secreted following LPS stimulation induced DC cell death. Apoptosis of mature DC required both NF-{kappa}B and STAT-1 activation, and was mediated through the induction of caspase-11 expression and activation of caspase-3. In vivo, we observed increased caspase-11 expression and a significant decrease in the number of splenic DC following LPS administration in wt, but not in STAT-1-deficient mice. Since mature DC are major contributors to the inflammatory response and essential partners in the induction of adaptive immunity, IFN{beta}-dependent elimination of activated DC could play an essential role in re-establishing homeostasis, and might represent a new molecular mechanism for the therapeutic effect of IFN{beta} in MS.


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J.-H. Yen, W. Kong, and D. Ganea
IFN-{beta} Inhibits Dendritic Cell Migration through STAT-1-Mediated Transcriptional Suppression of CCR7 and Matrix Metalloproteinase 9
J. Immunol., April 1, 2010; 184(7): 3478 - 3486.
[Abstract] [Full Text] [PDF]


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