Antifungal Activity of Plasmacytoid Dendritic Cells against Cryptococcus neoformans In Vitro Requires Expression of Dectin-3 (CLEC4D) and Reactive Oxygen Species
Abstract
Conventional dendritic cells (cDCs) are critical for protection against pulmonary infection with the opportunistic fungal pathogen Cryptococcus neoformans ; however, the role of plasmacytoid dendritic cells (pDCs) is unknown. We show for the first time that murine pDCs have direct activity against C. neoformans via reactive oxygen species (ROS), a mechanism different from that employed to control Aspergillus fumigatus infections. The anticryptococcal activity of murine pDCs is independent of opsonization but appears to require the C-type lectin receptor Dectin-3, a receptor not previously evaluated during cryptococcal infections. Human pDCs can also inhibit cryptococcal growth by a mechanism similar to that of murine pDCs. Experimental pulmonary infection of mice with a C. neoformans strain that induces protective immunity demonstrated that recruitment of pDCs to the lungs is CXCR3 dependent. Taken together, our results show that pDCs inhibit C. neoformans growth in vitro via the production of ROS and that Dectin-3 is required for optimal growth-inhibitory activity.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Sep 01, 2016
- Source ID
- 10.1128/iai.00103-16
Entities
People
- Althea Campuzano
- Andrew S. Mendiola
- Camaron R. Hole
- Chrissy M. Leopold Wager
- Floyd L. Wormley Jr.
- Karen L. Wozniak
- Xinsong Lin
Organizations
- Army Research Office
- National Institutes of Health
- University of Texas at Austin
- University of Texas at San Antonio