Abstract
The interactions of Candida species with host cells are crucial for candidiasis. Recognition and adherence to host constituents are the keys to initial colonization of mucosal surfaces and the invasion of host cells. Resistance to mucosal candidiasis is mediated by cell-mediated immunity. Knowledge about host receptors on immune cells and the adhesins on the surface of C. albicans are more redundant, respectively, than about the ligands on the fungal surface and the structures on the host cells bound by adhesions. Silencing or disrupting specific genes both in the pathogen and the host are developing optimistically. The research on IL-12/23 p40 knockout (KO) mice is sound in providing preliminary array data about the principal pathways in oral C. albicans infection and clues about the molecular differences between wild-type (WT) and p40 KO mice of candidiasis in different sites, thus, hints that certain specific drug targets accessible to topical agents for the clinical treatment of oral candidiasis and relevant mucocutaneous precancerous lesions.
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This work was supported by the Research and Development Program of Science & Technology, Hygiene Office in Zhejiang of China (2008C33026 and 2009A098).
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He, H., Cong, Y., Yang, H. et al. Mutative expression in Candida albicans infection and cytokine signaling network in gene knockout mice. Eur J Clin Microbiol Infect Dis 29, 913–916 (2010). https://doi.org/10.1007/s10096-010-0916-0
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DOI: https://doi.org/10.1007/s10096-010-0916-0