Dectin-1-Mediated DC-SIGN Recruitment to Candida albicans Contact Sites.

ABSTRACT: At host-pathogen contact sites with Candida albicans, Dectin-1 activates pro-inflammatory signaling, while DC-SIGN promotes adhesion to the fungal surface. We observed that Dectin-1 and DC-SIGN collaborate to enhance capture/retention of C. albicans under fluid shear culture conditions. Therefore, we devised a cellular model system wherein we could investigate the interaction between these two receptors during the earliest stages of host-pathogen interaction. In cells expressing both receptors, DC-SIGN was quickly recruited to contact sites (103.15% increase) but Dectin-1 did not similarly accumulate. Once inside the contact site, FRAP studies revealed a strong reduction in lateral mobility of DC-SIGN (but not Dectin-1), consistent with DC-SIGN engaging in multivalent adhesiv

SUBMITTER: Choraghe RP 

PROVIDER: S-EPMC7923000 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature