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Review

The role of pattern recognition receptors in the innate recognition of Candida albicans

, , , &
Pages 347-361 | Received 09 Oct 2014, Accepted 29 Jan 2015, Published online: 11 Jun 2015

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.

Table 2. Comparision of PRR-deficient mice and human PRRs genetic polymorphisms

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