ArticlePloS one2011
Type I interferon drives dendritic cell apoptosis via multiple BH3-only proteins following activation by PolyIC in vivo.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 63 citations in OpenAlex.
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- Perforin-2 is a pore-forming effector of endocytic escape in cross-presenting dendritic cells.Science (New York, N.Y.) · 2023Article
- Activation, Amplification, and Ablation as Dynamic Mechanisms of Dendritic Cell Maturation.Biology · 2023Review
- Life and death of tolerogenic dendritic cells.Trends in immunology · 2023Review
- Ablation of Adar1 in myeloid cells imprints a global antiviral state in the lung and heightens early immunity against SARS-CoV-2.Cell reports · 2023Article
- Stromal remodeling regulates dendritic cell abundance and activity in the tumor microenvironment.Cell reports · 2022Article
- TNF-α sculpts a maturation process in vivo by pruning tolerogenic dendritic cells.Cell reports · 2022Article
- Microbial (co)infections: Powerful immune influencers.PLoS pathogens · 2022Review
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- TLR3 Activation of Intratumoral CD103Frontiers in immunology · 2019Article
- The life and death of immune cell types: the role of BCL-2 anti-apoptotic molecules.Immunology and cell biology · 2017Review
- Murine Cytomegalovirus Disrupts Splenic Dendritic Cell SubsetsFrontiers in immunology · 2017Article
- Differential responses of normal human melanocytes to intra- and extracellular dsRNA.DNA and cell biology · 2015Article
- FcγRIIB prevents inflammatory type I IFN production from plasmacytoid dendritic cells during a viral memory response.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Prosurvival Bcl-2 family members reveal a distinct apoptotic identity between conventional and plasmacytoid dendritic cells.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Article
- Expansion of the neonatal platelet mass is achieved via an extension of platelet lifespan.Blood · 2014Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDC are activated by pathogen-associated molecular patterns (PAMPs), and this is pivotal for the induction of adaptive immune responses. Thereafter, the clearance of activated DC is crucial to prevent immune pathology. While PAMPs are of major interest for vaccine science due to their adjuvant potential, it is unclear whether and how PAMPs may affect DC viability. We aimed to elucidate the possible apoptotic mechanisms that control activated DC lifespan in response to PAMPs, particularly in vivo. METHODOLOGY/PRINCIPAL
findingsWe report that polyinosinic:polycytidylic acid (PolyIC, synthetic analogue of dsRNA) induces dramatic apoptosis of mouse splenic conventional DC (cDC) in vivo, predominantly affecting the CD8α subset, as shown by flow cytometry-based analysis of splenic DC subsets. Importantly, while Bim deficiency conferred only minor protection, cDC depletion was prevented in mice lacking Bim plus one of three other BH3-only proteins, either Puma, Noxa or Bid. Furthermore, we show that Type I Interferon (IFN) is necessary and sufficient for DC death both in vitro and in vivo, and that TLR3 and MAVS co-operate in IFNß production in vivo to induce DC death in response to PolyIC. CONCLUSIONS/SIGNIFICANCE: These results demonstrate for the first time in vivo that apoptosis restricts DC lifespan following activation by PolyIC, particularly affecting the CD8α cDC subset. Such DC apoptosis is mediated by the overlapping action of pro-apoptotic BH3-only proteins, including but not solely involving Bim, and is driven by Type I IFN. While Type I IFNs are important anti-viral factors, CD8α cDC are major cross-presenting cells and critical inducers of CTL. We discuss such paradoxical finding on DC death with PolyIC/Type I IFN. These results could contribute to understand immunosuppression associated with chronic infection, and to the optimization of DC-based therapies and the clinical use of PAMPs and Type I IFNs.
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