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- W2177788257 abstract "ABSTRACT The genetic basis of natural susceptibility to progressive Cryptococcus neoformans infection is not well understood. Using C57BL/6 and CBA/J inbred mice, we previously identified three chromosomal regions associated with C. neoformans susceptibility ( Cnes1 , Cnes2 , and Cnes3 ). To validate and characterize the role of Cnes2 during the host response, we constructed a congenic strain on the C57BL/6 background (B6.CBA- Cnes2 ). Phenotypic analysis of B6.CBA- Cnes2 mice 35 days after C. neoformans infection showed a significant reduction of fungal burden in the lungs and spleen with higher pulmonary expression of gamma interferon (IFN-γ) and interleukin-12 (IL-12), lower expression of IL-4, IL-5, and IL-13, and an absence of airway epithelial mucus production compared to that in C57BL/6 mice. Multiparameter flow cytometry of infected lungs also showed a significantly higher number of neutrophils, exudate macrophages, CD11b + dendritic cells, and CD4 + cells in B6.CBA- Cnes2 than in C57BL/6 mice. The activation state of recruited macrophages and dendritic cells was also significantly increased in B6.CBA- Cnes2 mice. Taken together, these findings demonstrate that the Cnes2 interval is a potent regulator of host defense, immune responsiveness, and differential Th1/Th2 polarization following C. neoformans infection." @default.
- W2177788257 created "2016-06-24" @default.
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- W2177788257 creator A5052174808 @default.
- W2177788257 date "2015-12-01" @default.
- W2177788257 modified "2023-10-16" @default.
- W2177788257 title "The<i>Cnes2</i>Locus on Mouse Chromosome 17 Regulates Host Defense against Cryptococcal Infection through Pleiotropic Effects on Host Immunity" @default.
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- W2177788257 doi "https://doi.org/10.1128/iai.00697-15" @default.
- W2177788257 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4645399" @default.
- W2177788257 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26371125" @default.
- W2177788257 hasPublicationYear "2015" @default.
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