ArticleScientific reports2016
Carboxyl-terminal fusion of E7 into Flagellin shifts TLR5 activation to NLRC4/NAIP5 activation and induces TLR5-independent anti-tumor immunity.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Flagellins as Vaccine Adjuvants and Cancer Immunotherapy: Recent Advances and Future Prospects.Immunology · 2025Review
- Natural compounds and programmed necrosis: pioneering a new frontier in cancer treatments.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Molecular mechanisms of pyroptosis and its role in anti-tumor immunity.International journal of biological sciences · 2023Review
- The Role of Programmed Necrosis in Colorectal Cancer.Cancers · 2022Review
- Targeting Xcr1 on Dendritic Cells Rapidly Induce Th1-Associated Immune Responses That Contribute to Protection Against Influenza Infection.Frontiers in immunology · 2022Article
- Physiopathology and effectiveness of therapeutic vaccines against human papillomavirus.Environmental science and pollution research international · 2021Review
- Inflammasomes and adaptive immune responses.Nature immunology · 2021Review
- Enhancement of antigen-specific humoral immune responses and protein solubility through conjugation of bacterial flagellin,Journal of veterinary science · 2019Article
- Chemical and Immunological Characteristics of Aluminum-Based, Oil-Water Emulsion, and Bacterial-Origin Adjuvants.Journal of immunology research · 2019Review
- Article
- Broad detection of bacterial type III secretion system and flagellin proteins by the human NAIP/NLRC4 inflammasome.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Flagellin has the capacity to activate both Toll-like receptor 5 (TLR5) and Nod-like receptor C4 (NLRC4)/neuronal apoptosis inhibitory protein 5 (NAIP5) inflammasome signaling. We fused E7m (the inactivated E7 of human papillomavirus) to either end of the flagellin protein, and the resulting recombinant flagellin-E7m proteins (rFliCE7m and rE7mFliC) were used as immunogens. Both fusion proteins activated receptor signaling to different degrees. rE7mFliC-induced TLR5 activity was 10-fold higher than that of rFliCE7m, whereas rFliCE7m activated the NLRC4/NAIP5 pathway more strongly. Therefore, these recombinant proteins provided a tool to investigate which signaling pathway is critical for the induction of antigen-specific T cell responses and anti-tumor immunity. We demonstrated that rFliCE7m induced higher levels of E7-specific IFN-gamma-secreting cells and cytotoxic T lymphocytes (CTLs) than rE7mFliC, and a single injection with rFliCE7m but not rE7mFliC inhibited E7-expressing tumor growth in vivo. Furthermore, we confirmed that CD8(+) T cells played a major role in the anti-tumor immunity induced by rFliCE7m. These findings suggested that the NLRC4/NAIP5 intracellular signaling pathway was critical for the induction of anti-tumor immunity. These observations provide important information for the rational design of flagellin-based immunotherapy.
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