Author
Listed:
- Xiaoming Sun
(Massachusetts General Hospital)
- Stephane Hua
(Massachusetts General Hospital)
- Ce Gao
(Massachusetts General Hospital)
- Jane E. Blackmer
(Massachusetts General Hospital)
- Zhengyu Ouyang
(Massachusetts General Hospital)
- Kevin Ard
(Massachusetts General Hospital)
- Andrea Ciaranello
(Massachusetts General Hospital)
- Sigal Yawetz
(Brigham and Women’s Hospital)
- Paul E. Sax
(Brigham and Women’s Hospital)
- Eric S. Rosenberg
(Massachusetts General Hospital)
- Mathias Lichterfeld
(Massachusetts General Hospital
Brigham and Women’s Hospital)
- Xu G. Yu
(Massachusetts General Hospital
Brigham and Women’s Hospital)
Abstract
Zika virus (ZIKV) is a mosquito-borne pathogen with increasing public health significance. To characterize immune responses to ZIKV, here we examine transcriptional signatures of CD4 T, CD8 T, B, and NK cells, monocytes, myeloid dendritic cells (mDCs), and plasmacytoid dendritic cells (pDCs) from three individuals with ZIKV infection. While gene expression patterns from most cell subsets display signs of impaired antiviral immune activity, pDCs from infected host have distinct transcriptional response associated with activation of innate immune recognition and type I interferon signaling pathways, but downregulation of key host factors known to support ZIKV replication steps; meanwhile, pDCs exhibit a unique expression pattern of gene modules that are correlated with alternative cell populations, suggesting collaborative interactions between pDCs and other immune cells, particularly B cells. Together, these results point towards a discrete but integrative function of pDCs in the human immune responses to ZIKV infection.
Suggested Citation
Xiaoming Sun & Stephane Hua & Ce Gao & Jane E. Blackmer & Zhengyu Ouyang & Kevin Ard & Andrea Ciaranello & Sigal Yawetz & Paul E. Sax & Eric S. Rosenberg & Mathias Lichterfeld & Xu G. Yu, 2020.
"Immune-profiling of ZIKV-infected patients identifies a distinct function of plasmacytoid dendritic cells for immune cross-regulation,"
Nature Communications, Nature, vol. 11(1), pages 1-13, December.
Handle:
RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-16217-5
DOI: 10.1038/s41467-020-16217-5
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