Inflammation Program, University of Iowa Carver College of Medicine, Iowa City, IA 52242, USA.
J Immunol. 2012 Nov 15;189(10):4713-7. doi: 10.4049/jimmunol.1201715. Epub 2012 Oct 15.
Nucleotide-binding domain leucine-rich repeat containing receptors (NLRs) are cytosolic receptors that initiate immune responses to sterile and infectious insults to the host. Studies demonstrated that Nlrp3 is critical for the control of Candida albicans infections and in the generation of antifungal Th17 responses. In this article, we show that the NLR family member Nlrp10 also plays a unique role in the control of disseminated C. albicans infection in vivo. Nlrp10-deficient mice had increased susceptibility to disseminated candidiasis, as indicated by decreased survival and increased fungal burdens. In contrast to Nlrp3, Nlrp10 deficiency did not affect innate proinflammatory cytokine production from macrophages and dendritic cells challenged with C. albicans. However, Nlrp10-deficient mice displayed a profound defect in Candida-specific Th1 and Th17 responses. These results demonstrate a novel role for Nlrp10 in the generation of adaptive immune responses to fungal infection.
核苷酸结合域富含亮氨酸重复受体(NLRs)是胞质受体,可引发宿主对无菌和感染性损伤的免疫反应。研究表明,Nlrp3 对于控制白色念珠菌感染和产生抗真菌 Th17 反应至关重要。在本文中,我们表明 NLR 家族成员 Nlrp10 也在体内控制白色念珠菌播散感染中发挥独特作用。Nlrp10 缺陷型小鼠对播散性念珠菌病的易感性增加,表现为存活率降低和真菌负荷增加。与 Nlrp3 不同,Nlrp10 缺陷型小鼠在受到白色念珠菌刺激时,巨噬细胞和树突状细胞中先天促炎细胞因子的产生不受影响。然而,Nlrp10 缺陷型小鼠在白色念珠菌特异性 Th1 和 Th17 反应中表现出严重缺陷。这些结果表明 Nlrp10 在产生针对真菌感染的适应性免疫反应中具有新的作用。