ArticleCell death & disease2016
TLR and NLRP3 inflammasome-dependent innate immune responses to tumor-derived autophagosomes (DRibbles).
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 47 citations in OpenAlex.
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- Long noncoding RNA PARAL1 regulates myeloid dendritic cell differentiation and TLR signaling.Genes and immunity · 2025Article
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- Whole tumour cell-based vaccines: tuning the instruments to orchestrate an optimal antitumour immune response.British journal of cancer · 2023Review
- A C-type lectin induces NLRP3 inflammasome activation via TLR4 interaction in human peripheral blood mononuclear cells.Cellular and molecular life sciences : CMLS · 2023Article
- PHLDA1 modulates microglial response and NLRP3 inflammasome signaling following experimental subarachnoid hemorrhage.Frontiers in immunology · 2023Article
- Inhibition of Schwann Cell Pyroptosis Promotes Nerve Regeneration in Peripheral Nerve Injury in Rats.Mediators of inflammation · 2023Article
- Lung Inflammasome Activation in SARS-CoV-2 Post-Mortem Biopsies.International journal of molecular sciences · 2022Article
- Caspase-1 Inhibition Reduces Occurrence of PANoptosis in Macrophages Infected byJournal of clinical medicine · 2022Article
- Anti‑βInternational journal of molecular medicine · 2022Article
- Inflammasome NLRP3 activation induced by Convulxin, a C-type lectin-like isolated from Crotalus durissus terrificus snake venom.Scientific reports · 2022Article
- Regulation of autophagy fires up the cold tumor microenvironment to improve cancer immunotherapy.Frontiers in immunology · 2022Review
- FMDV Leader Protein Interacts with the NACHT and LRR Domains of NLRP3 to Promote IL-1β Production.Viruses · 2021Article
- Rab GTPase Mediating Regulation of NALP3 in Colorectal Cancer.Molecules (Basel, Switzerland) · 2020Article
- NLRP3 played a role in Trichinella spiralis-triggered Th2 and regulatory T cells response.Veterinary research · 2020Article
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- Unraveling the regulatory role of endoplasmic-reticulum-associated degradation in tumor immunity.Critical reviews in biochemistry and molecular biology · 2020Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagosomes derived from tumor cells, also referred to as defective ribosomal products in blebs (DRibbles), have been previously shown to stimulate potent T-cell responses and mediate tumor regression when used as therapeutic cancer vaccines in multiple preclinical cancer models. In this report, we investigated the underlining mechanisms by which DRibbles induced T-cell activation, particularly how DRibbles activated antigen-presenting cells (APCs). We found that DRibbles could induce a rapid differentiation of monocytes and DC precursor (pre-DC) cells into functional APCs. DRibbles triggered innate receptor signaling via Toll-like Receptors (TLR)-2, TLR4, TLR7, TLR8, and nucleotide-binding oligomerization domain-containing protein 2 (NOD2), but not TLR3, TLR5, or TLR9. DRibbles induced PBMCs to produce pro-inflammatory cytokines, such as IL-6, IL-10, TNF-α, and IL-1β. DRibbles induced IL-1β release from PBMC or THP-1 cells without LPS priming, but required the core machinery of NLRP3 inflammasomes. Active endocytosis was required for inflammasome activation and cross presentation, and blocking endosome acidification or the ER-associated degradation (ERAD) pathway resulted in opposite effects on these two processes. Our data show that DRibbles could induce strong innate immune responses via multiple pattern recognition receptors, and explain why DRibbles could function as excellent antigen carriers to induce adaptive immune responses to both tumor cells and viruses. In contrast to the well-established inhibitory effect of autophagy on the inflammasome activation of APCs, our study demonstrates that isolated autophagosomes (DRibbles) from antigen donor cells activate inflammasomes by providing first and second signals required for IL-1β production by PMBC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.