The Journal of Experimental Medicine
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Published 5 May 2003. doi:10.1084/jem.20021258
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© Rockefeller University Press, 0022-1007/2003/5/1213 $5.00
The Journal of Experimental Medicine, Volume 197, Number 9, 1213-1219

Brief Definitive Report

Deficiencies of GM-CSF and Interferon {gamma} Link Inflammation and Cancer

Thomas Enzler1, Silke Gillessen1, John P. Manis2, David Ferguson2, James Fleming2, Frederick W. Alt2, Martin Mihm3 and Glenn Dranoff1

1 Department of Medical Oncology, Dana-Farber Cancer Institute and Department of Medicine, Brigham and Women's Hospital and Harvard Medical School
2 Howard Hughes Medical Institute and Children's Hospital, Center for Blood Research and Department of Genetics, Harvard Medical School, Boston, MA 02115
3 Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114

Address correspondence to G. Dranoff, Dana-Farber Cancer Institute, Dana 510E, 44 Binney St., Boston, MA 02115. Phone: 617-632-5051; Fax: 617-632-5167; E-mail: glenn_dranoff{at}dfci.harvard.edu

Chronic inflammation contributes to carcinogenesis, but the underlying mechanisms are poorly understood. We report that aged granulocyte-macrophage colony stimulating factor (GM-CSF)-deficient mice develop a systemic lupus erythematosis (SLE)-like disorder associated with the impaired phagocytosis of apoptotic cells. Concurrent deficiency of interferon (IFN)-{gamma} attenuates the SLE, but promotes the formation of diverse hematologic and solid neoplasms within a background of persistent infection and inflammation. Whereas activated B cells show a resistance to fas-induced apoptosis, antimicrobial therapy prevents lymphomagenesis and solid tumor development. These findings demonstrate that the interplay of infectious agents with cytokine-mediated regulation of immune homeostasis is a critical determinant of cancer susceptibility.

Key Words: GM-CSF • IFN-{gamma} • cancer • inflammation • SLE


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