Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0006849 (oral candidiasis)
 1,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oral candidiasis is a significant health problem in terms of both morbidity and economic outlay. Infections are predominantly caused by the commensal C. albicans, and affect immunocompromised individuals, including HIV-positive and AIDS patients, organ transplant recipients and chemotherapy patients. The molecular and cellular immune mechanisms involved in protection from and responses to oral candidiasis are overlapping, but distinct from those associated with other manifestations of the disease, including systemic, vaginal and gastric candidiasis. In oral candidiasis, clinical observations and experimental mouse models suggest a critical role for cell-mediated immunity. In mice, CD4+ T-cells and the p40 subunit of interleukins 12 and 23 are strict prerequisites for resistance; however abrogation of IFN-gamma does not confer susceptibility. Here, we discuss this apparent inconsistency, and review the experimental evidence that clarifies which immune pathways are specifically involved in resistance and responses to candidiasis of the oral cavity. We also highlight deficiencies in the literature, particularly concerning the putative roles of some relatively new elements in immunobiology: interleukin-23, interleukin-17 and T helper (Th)17 cells.
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PMID:Cellular and molecular mechanisms of resistance to oral Candida albicans infections. 1850 91

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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PMID:Mutative expression in Candida albicans infection and cytokine signaling network in gene knockout mice. 2038 86