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• W2039836807 abstract "We inoculated BALB/c mice deficient in STAT6 (STAT6(-/-)) and their wild-type (wt) littermates (STAT6(+/+)) with the natural mouse pathogen, ectromelia virus (EV). STAT6(-/-) mice exhibited increased resistance to generalized infection with EV when compared with STAT6(+/+) mice. In the spleens and lymph nodes of STAT6(-/-) mice, T helper 1 (Th1) cytokines were induced at earlier time points and at higher levels postinfection when compared with those in STAT6(+/+) mice. Elevated levels of NO were evident in plasma and splenocyte cultures of EV-infected STAT6(-/-) mice in comparison with STAT6(+/+) mice. The induction of high levels of Th1 cytokines in the mutant mice correlated with a strong natural killer cell response. We demonstrate in genetically susceptible BALB/c mice that the STAT6 locus is critical for progression of EV infection. Furthermore, in the absence of this transcription factor, the immune system defaults toward a protective Th1-like response, conferring pronounced resistance to EV infection and disease progression." @default.
• W2039836807 created "2016-06-24" @default.
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• W2039836807 date "2001-05-22" @default.
• W2039836807 modified "2023-10-01" @default.
• W2039836807 title "Enhanced resistance in STAT6-deficient mice to infection with ectromelia virus" @default.
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• W2039836807 doi "https://doi.org/10.1073/pnas.111151098" @default.
• W2039836807 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/34435" @default.
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• W2039836807 hasPublicationYear "2001" @default.
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