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B Protein Bcl-3 Negatively Regulates Transcription of the IL-10 Gene in Macrophages1
* Department of Internal Medicine II and
Institute of Medical Microbiology, Immunology and Hygiene, Technical University of Munich, Munich, Germany;
Department of Pediatrics, University of Ulm, Ulm, Germany; and
Institute of Medical Microbiology, University of Düsseldorf, Düsseldorf, Germany
NF-
B/Rel transcription factors, implicated in inflammatory and immune responses against pathogens, are regulated by IB proteins. The physiological and molecular function of the IB family member Bcl-3 is understood only poorly. In this study, the role of Bcl-3 in an innate immune response was examined by gene targeting. We demonstrate that Bcl-3–/– mice are highly susceptible to Listeria monocytogenes infection. This correlates with diminished production of IL-12 p70 and IFN-
in vivo, which is mainly due to elevated synthesis of IL-10. Isolated peritoneal macrophages from Bcl-3–/– mice also produce elevated amounts of IL-10, which inhibit IL-12 p70 synthesis in an autocrine fashion. Thus, these data establish Bcl-3 as an inhibitor of IL-10 expression in macrophages. Furthermore, we show that Bcl-3 is not implicated in IL-10 mRNA stabilization but regulates the initiation of IL-10 transcription. Taken together, our results show that an essential function of Bcl-3 during an innate immune response against bacteria is to inhibit transcription of the IL-10 gene in macrophages.
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