Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 200, Issue 4, Pages 437-445Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20040712
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Funding
- NCI NIH HHS [R01 CA87924, R01 CA087924] Funding Source: Medline
- NCRR NIH HHS [S10 RR15862-01] Funding Source: Medline
- NIAID NIH HHS [R01 AI056154, R37 AI047868, R37 AI47868] Funding Source: Medline
- NIGMS NIH HHS [GM 08042, T32 GM007185, GM 07185, GM 07104, T32 GM008042, T32 GM007104] Funding Source: Medline
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Numerous bacterial products such as lipopolysaccharide potently induce type I interferons (lFNs); however, the contribution of this innate response to host defense against bacterial infection remains unclear. Although mice deficient in either IFN regulatory factor (IR-F)3 or the type I IFN receptor (IFNAR)1 are highly susceptible to viral infection, we show that these mice exhibit a profound resistance to infection caused by the Gram-positive intracellular bacterium Listeria monocytogenes compared with wild-type controls. Furthermore, this enhanced bacterial clearance is accompanied by a block in L. monocytogenes-induced splenic apoptosis in IRF3- and IFNAR1-deficient mice. Thus, our results highlight the disparate roles of type I IFNs during bacterial versus viral infections and stress the importance of proper IFN modulation in host defense.
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