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Dendritic cells (DCs) abundantly express diverse receptors to recognize mannans in the outer surface of  Candida  cell wall, and these interactions dictate the host immune responses that determine disease outcomes.  C. krusei  prevalence in candidiasis worldwide has increased since this pathogen has developed multidrug resistance. However, little is known how the immune system responds to  C. krusei . Particularly, the molecular mechanisms of the interplay between  C. krusei  mannan and DCs remain to be elucidated. We investigated how  C. krusei  mannan affected DC responses in comparison to  C. albicans ,  C. tropicalis  and  C. glabrata  mannan. Our results showed that only  C. krusei  mannan induced massive cytokine responses in DCs, and led to apoptosis. Although  C. krusei  mannan-activated DCs underwent apoptosis, they were still capable of initiating Th17 response.  C. krusei  mannan-mediated DC apoptosis was obligated to the TLR2 and MyD88 pathway. These pathways also controlled Th1/Th17 switching possibly by virtue of the production of the polarizing cytokines IL-12 and IL-6 by the  C. krusei  mannan activated-DCs. Our study suggests that TLR2 and MyD88 pathway in DCs are dominant for  C. krusei  mannan recognition, which differs from the previous reports showing a crucial role of C-type lectin receptors in  Candida  mannan sensing.

Cell wall mannan of Candida krusei mediates dendritic cell apoptosis and orchestrates Th17 polarization via TLR-2/MyD88-dependent pathway