Journal
IMMUNITY
Volume 36, Issue 2, Pages 166-174Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2012.01.011
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Funding
- Leukemia and Lymphoma society
- Cancer Research Institute Predoctoral Emphasis in Tumor Immunology Scholarship
- NHMRC
- Susan G. Komen Breast Cancer Foundation
- Prostate Cancer Foundation of Australia, Cancer Council Victoria
- Leukemia Foundation of Australia, Victorian Breast Cancer Research Consortium, Victorian Cancer Agency
- Australian Rotary Health Foundation
- National Institutes of Health [R01Al28900, U54AI057158]
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Interferons (IFNs) were discovered as cytokines induced during and protecting from viral infection. They have been documented to play essential roles in numerous physiological processes beyond antiviral and antimicrobial defense, including immunomodulation, cell cycle regulation, cell survival, and cell differentiation. Recent data have also uncovered a potentially darker side to IFN, including roles in inflammatory diseases, such as autoimmunity and diabetes. IFN can have effects in the absence of acute infection, highlighting a physiologic role for constitutive IFN. Type I IFNs are constitutively produced at vanishingly low quantities and yet exert profound effects, mediated in part through modulation of signaling intermediates required for responses to diverse cytokines. We review evidence for a yin-yang of IFN function through its role in modulating crosstalk between multiple cytokines by both feedforward and feedback regulation of common signaling intermediates and postulate a homeostatic role for IFN through tonic signaling in the absence of acute infection.
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