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• W2131818384 startingPage "37" @default.
• W2131818384 abstract "To define the immunological functions of tumor necrosis factor (TNF) in Candida albicans infection, TNF/lymphotoxin (LT)-alpha double-deficient mice were assessed for susceptibility to systemic or gastrointestinal infection and parameters of innate and adaptive Th immunity. When compared to wild-type mice, TNF/LT-alpha-deficient mice were more susceptible to either type of infection caused by virulent or low-virulence C. albicans cells. Susceptibility to infection correlated with impaired development of protective Th1 responses, in spite of the production of bioactive IL-12. The occurrence of predominant Th2 responses was associated with both impaired antifungal effector functions of neutrophils and a defective expression of co-stimulatory molecules on macrophages. All functions were improved upon administration of recombinant TNF-alpha, also resulting in increased resistance to infection. These findings indicate that the protective effect of TNF-alpha in candidiasis relies on the induction of antifungal Th1 responses, possibly occurring through stimulation of antifungal effector functions and co-stimulatory activities of phagocytic cells." @default.
• W2131818384 created "2016-06-24" @default.
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• W2131818384 date "1998-01-01" @default.
• W2131818384 modified "2023-09-27" @default.
• W2131818384 title "Defective co-stimulation and impaired Th1 development in tumor necrosis factor/lymphotoxin-alpha double-deficient mice infected with Candida albicans" @default.
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• W2131818384 doi "https://doi.org/10.1093/intimm/10.1.37" @default.
• W2131818384 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9488154" @default.
• W2131818384 hasPublicationYear "1998" @default.
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