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The genetic basis of natural susceptibility to progressiveCryptococcus neoformans infection is not well understood. Using C57BL/6 and CBA/J inbred mice, we previously identified three chromosomal regions associated withC. neoformans susceptibility (Cnes1 ,Cnes2 , andCnes3 ). To validate and characterize the role ofCnes2 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 afterC. 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 theCnes2 interval is a potent regulator of host defense, immune responsiveness, and differential Th1/Th2 polarization followingC. neoformans infection.

TheCnes2Locus on Mouse Chromosome 17 Regulates Host Defense against Cryptococcal Infection through Pleiotropic Effects on Host Immunity