Complement receptor 3-dependent engagement by Candida glabrata β-glucan modulates dendritic cells to induce regulatory T-cell expansion

is an important pathogen causing invasive infection associated with a high mortality rate. One mechanism that causes the failure of eradication is an increase in regulatory T cells (Treg), which play a major role in immune suppression and promoting pathogenicity. To date, how induces a Treg response remains unclear. Dendritic cells (DCs) recognition of fungi provides the fundamental signal determining the fate of the T-cell response. This study investigated the interplay between and DCs and its effect on Treg induction. We found that β-glucan was a major component that interacted with DCs and consequently mediated the Treg response. Blocking the binding of β-glucan to dectin-1 and complement receptor 3 (CR3) showed that CR3 activation in DCs was crucial for the induction of Treg. Furthermore, a ligand-receptor binding assay showed the preferential binding of β-glucan to CR3. Our data suggest that β-glucan potentially mediates the Treg response, probably through CR3-dependent activation in DCs. This study contributes new insights into immune modulation by that may lead to a better design of novel immunotherapeutic strategies for invasive infection.