Modulation of the Candida albicans-induced immune response by the ITIM-coupled receptor CLEC-12A (A05)

项目A5的重点是模式识别受体(PRR)介导的调节真菌诱导的宿主免疫反应的作用。白念珠菌与髓系抑制性C型凝集素受体CLEC-12A结合，可下调白念珠菌诱导的单核细胞分泌细胞因子，降低Dectin-1介导的免疫应答。A5将在体外和小鼠感染模型中阐明ITIM偶联CLEC-12A介导的白色念珠菌免疫反应调节的机制。这将包括确定CLEC-12A对肠道微生物组的作用，以及评估CLEC-12A表达作为潜在的诊断标记物。

Project A5 focuses on the role of the pattern-recognition receptor (PRR)-mediated modulation of the fungal-induced immune responses of the host. C. albicans binding to the myeloid inhibitory C-type lectin receptor CLEC-12A downregulates C. albicans-induced cytokine secretion by monocytes and decreased Dectin-1-mediated immune response. A5 will elucidate the mechanisms of ITIM-coupled CLEC-12A-mediated regulation of C. albicans immune responses in vitro and in a mouse infection model. This will include defining the role of CLEC-12A on the gut microbiome as well as evaluating CLEC-12A expression as a potential diagnostic marker.