کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3421924 | 1226698 | 2013 | 8 صفحه PDF | دانلود رایگان |

• Many fungi bind to receptors on host cells and thereby induce their own uptake.
• Inhibiting Candida albicans interaction with EGFR–HER2 reduces oropharyngeal infection.
• Blocking binding of Rhizopus oryzae to GRP78 protects against lethal mucormycosis.
• Targeting host cell receptors for fungi is a promising therapeutic strategy.
The invasion and stimulation of normally non-phagocytic host cells, such as epithelial and endothelial cells, is a key step in the pathogenesis of many fungal infections. In most cases, host cell invasion and/or stimulation of a proinflammatory response is induced when proteins or carbohydrates on the fungal cell surface bind to receptors on the host cell. Although many of these fungal–host cell interactions have only been investigated in vitro, the therapeutic efficacy of blocking the host cell receptors for Candida albicans and Rhizopus oryzae has been demonstrated in experimental animal models of infection. We summarize recent studies of the fungal receptors on normally non-phagocytic host cells and the therapeutic implications of blocking these receptors.
Journal: - Volume 21, Issue 8, August 2013, Pages 389–396