Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 121, Issue 6, Pages 2436-2446Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI44796
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Funding
- National Institute on Aging [F30AG030298]
- Margaret A. Cunningham Immune Mechanisms of Cancer Research Fellowship
- American Lung Association, United Against Lung Cancer
- NIH [R01 CA122794, R01 CA140594, R01 CA143083]
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Lung cancer is the leading cause of cancer death worldwide. Both principal factors known to cause lung cancer, cigarette smoke and asbestos, induce pulmonary inflammation, and pulmonary inflammation has recently been implicated in several murine models of lung cancer. To further investigate the role of inflammation in the development of lung cancer, we generated mice with combined loss of IFN-gamma and the beta-common cytokines GM-CSF and IL-3. These immunodeficient mice develop chronic pulmonary inflammation and lung tumors at a high frequency. Examination of the relationship between these tumors and their inflammatory microenvironment revealed a dual role for the immune system in tumor development. The inflammatory cytokine IL-6 promoted optimal tumor growth, yet wild-type mice rejected transplanted tumors through the induction of adaptive immunity. These findings suggest a model whereby cytokine deficiency leads to oncogenic inflammation that combines with defective antitumor immunity to promote lung tumor formation, representing a unique system for studying the role of the immune system in lung tumor development.
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