Journal
JOURNAL OF IMMUNOLOGY
Volume 195, Issue 1, Pages 210-216Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1401139
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Funding
- National Institutes of Health [AI 058211, AI096088, 5T32 AI07525, 5T32 DK007328, AI082185]
- Fonds zur Forderung der Wissenschaftlichen Forschung [SFB-28, W1220-B09]
- Austrian Science Fund (FWF) [F 2802] Funding Source: researchfish
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IFNs, which transduce pivotal signals through Stat1 and Stat2, effectively suppress the replication of Legionella pneumophila in primary murine macrophages. Although the ability of IFN-gamma to impede L. pneumophila growth is fully dependent on Stat1, IFN-alpha beta unexpectedly suppresses L. pneumophila growth in both Stat1- and Stat2-deficient macrophages. New studies demonstrating that the robust response to IFN-alpha beta is lost in Stat1-Stat2 double-knockout macrophages suggest that Stat1 and Stat2 are functionally redundant in their ability to direct an innate response toward L. pneumophila. Because the ability of IFN-alpha beta to signal through Stat1-dependent complexes (i.e., Stat1-Stat1 and Stat1-Stat2 dimers) has been well characterized, the current studies focus on how Stat2 is able to direct a potent response to IFN-alpha beta in the absence of Stat1. These studies reveal that IFN-alpha beta is able to drive the formation of a Stat2 and IFN regulatory factor 9 complex that drives the expression of a subset of IFN-stimulated genes, but with substantially delayed kinetics. These observations raise the possibility that this pathway evolved in response to microbes that have devised strategies to subvert Stat1-dependent responses.
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