Complement receptor 3-dependent engagement by Candida glabrata β-glucan modulates dendritic cells to induce regulatory T-cell expansion
Areerat Kunanopparat,
Truc Thi Huong Dinh,
Pranpariya Ponpakdee,
Panuwat Padungros,
Warerat Kaewduangduen,
Kasirapat Ariya-anandech,
Phawida Tummamunkong,
Amanee Samaeng,
Pannagorn Sae-ear,
Asada Leelahavanichkul,
Nattiya Hirankarn,
Patcharee Ritprajak
Affiliations
Areerat Kunanopparat
Department of Microbiology, Faculty of Dentistry, Center of Excellence in Integrative Immuno-Microbial Biochemistry and Bioresponsive Nanomaterials, Chulalongkorn University , Bangkok, Thailand
Truc Thi Huong Dinh
Department of Microbiology, Faculty of Dentistry, Center of Excellence in Integrative Immuno-Microbial Biochemistry and Bioresponsive Nanomaterials, Chulalongkorn University , Bangkok, Thailand
Pranpariya Ponpakdee
Department of Chemistry, Faculty of Science, Green Chemistry for Fine Chemical Production and Environmental Remediation Research Unit, Chulalongkorn University , Bangkok, Thailand
Panuwat Padungros
Department of Chemistry, Faculty of Science, Green Chemistry for Fine Chemical Production and Environmental Remediation Research Unit, Chulalongkorn University , Bangkok, Thailand
Warerat Kaewduangduen
Department of Microbiology, Faculty of Dentistry, Center of Excellence in Integrative Immuno-Microbial Biochemistry and Bioresponsive Nanomaterials, Chulalongkorn University , Bangkok, Thailand
Kasirapat Ariya-anandech
Department of Microbiology, Faculty of Dentistry, Center of Excellence in Integrative Immuno-Microbial Biochemistry and Bioresponsive Nanomaterials, Chulalongkorn University , Bangkok, Thailand
Phawida Tummamunkong
Department of Microbiology, Faculty of Dentistry, Center of Excellence in Integrative Immuno-Microbial Biochemistry and Bioresponsive Nanomaterials, Chulalongkorn University , Bangkok, Thailand
Amanee Samaeng
Department of Microbiology, Faculty of Dentistry, Center of Excellence in Integrative Immuno-Microbial Biochemistry and Bioresponsive Nanomaterials, Chulalongkorn University , Bangkok, Thailand
Pannagorn Sae-ear
Faculty of Dentistry, Oral Biology Research Center, Chulalongkorn University , Bangkok, Thailand
Asada Leelahavanichkul
Department of Microbiology, Faculty of Medicine, Center of Excellence in Translational Research in Inflammation and Immunology (CETRII), Chulalongkorn University , Bangkok, Thailand
Nattiya Hirankarn
Center of Excellence in Immunology and Immune-Mediated Diseases, Faculty of Medicine, Chulalongkorn University , Bangkok, Thailand
Patcharee Ritprajak
Department of Microbiology, Faculty of Dentistry, Center of Excellence in Integrative Immuno-Microbial Biochemistry and Bioresponsive Nanomaterials, Chulalongkorn University , Bangkok, Thailand
Candida glabrata is an important pathogen causing invasive infection associated with a high mortality rate. One mechanism that causes the failure of Candida eradication is an increase in regulatory T cells (Treg), which play a major role in immune suppression and promoting Candida pathogenicity. To date, how C. glabrata 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 C. glabrata and DCs and its effect on Treg induction. We found that C. glabrata β-glucan was a major component that interacted with DCs and consequently mediated the Treg response. Blocking the binding of C. glabrata 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 C. glabrata β-glucan to CR3. Our data suggest that C. glabrata β-glucan potentially mediates the Treg response, probably through CR3-dependent activation in DCs. This study contributes new insights into immune modulation by C. glabrata that may lead to a better design of novel immunotherapeutic strategies for invasive C. glabrata infection.
