| Literature DB >> 29203862 |
Solana G Alculumbre1,2, Violaine Saint-André1,3, Jeremy Di Domizio4, Pablo Vargas1,5, Philemon Sirven1,2, Pierre Bost1,2,6, Mathieu Maurin1,2, Paolo Maiuri1,7, Maxime Wery1,3, Mabel San Roman1,2, Léa Savey8,9, Maxime Touzot10, Benjamin Terrier11, David Saadoun8,9, Curdin Conrad4, Michel Gilliet4, Antonin Morillon1,3, Vassili Soumelis12,13,14.
Abstract
Innate immune cells adjust to microbial and inflammatory stimuli through a process termed environmental plasticity, which links a given individual stimulus to a unique activated state. Here, we report that activation of human plasmacytoid predendritic cells (pDCs) with a single microbial or cytokine stimulus triggers cell diversification into three stable subpopulations (P1-P3). P1-pDCs (PD-L1+CD80-) displayed a plasmacytoid morphology and specialization for type I interferon production. P3-pDCs (PD-L1-CD80+) adopted a dendritic morphology and adaptive immune functions. P2-pDCs (PD-L1+CD80+) displayed both innate and adaptive functions. Each subpopulation expressed a specific coding- and long-noncoding-RNA signature and was stable after secondary stimulation. P1-pDCs were detected in samples from patients with lupus or psoriasis. pDC diversification was independent of cell divisions or preexisting heterogeneity within steady-state pDCs but was controlled by a TNF autocrine and/or paracrine communication loop. Our findings reveal a novel mechanism for diversity and division of labor in innate immune cells.Entities:
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Year: 2017 PMID： 29203862 DOI： 10.1038/s41590-017-0012-z
Source DB: PubMed Journal: Nat Immunol ISSN： 1529-2908 Impact factor: 25.606