| Literature DB >> 24981333 |
Marcin Kwissa1, Helder I Nakaya2, Nattawat Onlamoon3, Jens Wrammert4, Francois Villinger5, Guey Chuen Perng6, Sutee Yoksan7, Kovit Pattanapanyasat3, Kulkanya Chokephaibulkit8, Rafi Ahmed4, Bali Pulendran9.
Abstract
Dengue virus (DENV) infection induces the expansion of plasmablasts, which produce antibodies that can neutralize DENV but also enhance disease upon secondary infection with another DENV serotype. To understand how these immune responses are generated, we used a systems biological approach to analyze immune responses to dengue in humans. Transcriptomic analysis of whole blood revealed that genes encoding proinflammatory mediators and type I interferon-related proteins were associated with high DENV levels during initial symptomatic disease. Additionally, CD14(+)CD16(+) monocytes increased in the blood. Similarly, in a nonhuman primate model, DENV infection boosted CD14(+)CD16(+) monocyte numbers in the blood and lymph nodes. Upon DENV infection in vitro, monocytes upregulated CD16 and mediated differentiation of resting B cells to plasmablasts as well as immunoglobulin G (IgG) and IgM secretion. These findings provide a detailed picture of innate responses to dengue and highlight a role for CD14(+)CD16(+) monocytes in promoting plasmablast differentiation and anti-DENV antibody responses.Entities:
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Year: 2014 PMID： 24981333 PMCID： PMC4116428 DOI： 10.1016/j.chom.2014.06.001
Source DB: PubMed Journal: Cell Host Microbe ISSN： 1931-3128 Impact factor: 21.023