Figures & data
Table 1. Pattern recognition receptors and C. albicans PAMPs
Figure 1. Overview of PRRs for C. albicans recognition. Recognition of C. albicans is mainly mediated by Toll-like receptors (TLRs) and C-type lectin receptors (CLRs). (A) The recognition of C. albicans by some CLRs can stimulate receptor phosphorylation and recruitment of the spleen tyrosine kinase (SYK). The association of dectin-1 with SYK activates assembly of the CARD complex (CARD9, BCL-10 and MALT-1). This results in the release of NF-κB. Syk activation also induces the noncanonical NF-κB pathway mediated by NF-κB-inducing kinase (NIK). Only the Dectin-1 and DC-SIGN recruit Ras for signal transducing, which leads to the release of NF-κB. Dectin-1 recognition of C. albicans can also activate the NLRP3 inflammasome through a mechanism that involves Syk and ROS. (B) The recognition of C. albicans by some TLRs can stimulate MyD88-dependent or TRIF-dependent pathways, leading to the release of NF-κB or the activation of IRF3/7.
![Figure 1. Overview of PRRs for C. albicans recognition. Recognition of C. albicans is mainly mediated by Toll-like receptors (TLRs) and C-type lectin receptors (CLRs). (A) The recognition of C. albicans by some CLRs can stimulate receptor phosphorylation and recruitment of the spleen tyrosine kinase (SYK). The association of dectin-1 with SYK activates assembly of the CARD complex (CARD9, BCL-10 and MALT-1). This results in the release of NF-κB. Syk activation also induces the noncanonical NF-κB pathway mediated by NF-κB-inducing kinase (NIK). Only the Dectin-1 and DC-SIGN recruit Ras for signal transducing, which leads to the release of NF-κB. Dectin-1 recognition of C. albicans can also activate the NLRP3 inflammasome through a mechanism that involves Syk and ROS. (B) The recognition of C. albicans by some TLRs can stimulate MyD88-dependent or TRIF-dependent pathways, leading to the release of NF-κB or the activation of IRF3/7.](/cms/asset/28775536-1671-4730-a49c-5877f1d2b566/kvir_a_1014270_f0001_oc.gif)
Table 2. Comparision of PRR-deficient mice and human PRRs genetic polymorphisms