Antifungal Activity of Plasmacytoid Dendritic Cells against Cryptococcus neoformans In Vitro Requires Expression of Dectin-3 (CLEC4D) and Reactive Oxygen Species

被引:34
作者
Hole, Camaron R. [1 ,2 ]
Wager, Chrissy M. Leopold [1 ,2 ]
Mendiola, Andrew S. [1 ,2 ]
Wozniak, Karen L. [1 ,2 ]
Campuzano, Althea [1 ,2 ]
Lin, Xin [3 ,4 ]
Wormley, Floyd L., Jr. [1 ,2 ]
机构
[1] Univ Texas San Antonio, Dept Biol, San Antonio, TX 78249 USA
[2] Univ Texas San Antonio, South Texas Ctr Emerging Infect Dis, San Antonio, TX 78249 USA
[3] Univ Texas MD Anderson Canc Ctr, Dept Mol & Cellular Oncol, Houston, TX 77030 USA
[4] Univ Texas Grad Sch Biomed Sci, Canc Biol Program, Houston, TX USA
基金
美国国家卫生研究院;
关键词
PULMONARY CRYPTOCOCCOSIS; PROTECTIVE IMMUNITY; LECTIN RECEPTORS; HOST-DEFENSE; MURINE MODEL; MOUSE MODEL; MENINGITIS; INFECTION; RESPONSES; GAMMA;
D O I
10.1128/IAI.00103-16
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:2493 / 2504
页数:12
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