ArticleOncoimmunology2016
NLRC5 elicits antitumor immunity by enhancing processing and presentation of tumor antigens to CD8(+) T lymphocytes.
Article in Oncoimmunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 77 citations in OpenAlex.
- NLRC5-Deficient Macrophages Promote a Tumor-Permissive Phenotype via AXL- and MERTK-Mediated Efferocytosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- NLRC5 Deficiency Delays Bone Healing by Inhibiting Osteogenic Differentiation of Bone Marrow-Derived Stem Cells and Altering the Immune Microenvironment.International journal of molecular sciences · 2026Article
- NLRC5 expression within tumor cells is critical to activate adaptive and innate antitumor immune responses.Immunotherapy advances · 2026Article
- Cancer vaccine overcomes immune evasion of nasopharyngeal carcinoma by restoring MHC-I through transcriptional regulation of NLRC5.Journal of translational medicine · 2025Article
- ThemSphere · 2025Article
- LncRNA-CTD suppresses metastasis and immune evasion by modulating snail1 and MHC-I expression in colorectal cancer.Journal for immunotherapy of cancer · 2025Article
- Factors that increase class I MHC expression may contribute to the development of immune checkpoint inhibitor-induced diabetes.Journal for immunotherapy of cancer · 2025Article
- Risk score model with two immune infiltration-related long non-coding RNAs to predict prognosis in patients with osteosarcoma.Oncology letters · 2025Article
- New insights into the structure domain and function of NLR family CARD domain containing 5.Cell communication and signaling : CCS · 2025Review
- Pharmacological strategies to overcome immune checkpoint inhibitor resistance in non-small cell lung cancer.Frontiers in oncology · 2025Review
- Orientia tsutsugamushi Ank5 promotes NLRC5 cytoplasmic retention and degradation to inhibit MHC class I expression.Nature communications · 2024Article
- NLRC5 promotes endometrial carcinoma progression by regulating NF-κB pathway-mediated mismatch repair gene deficiency.Scientific reports · 2024Article
- Engineering Challenges and Opportunities in Autologous Cellular Cancer Immunotherapy.Journal of immunology (Baltimore, Md. : 1950) · 2024Review
- A Ménage à trois: NLRC5, immunity, and metabolism.Frontiers in immunology · 2024Review
- FAK suppresses antigen processing and presentation to promote immune evasion in pancreatic cancer.Gut · 2023Article
- Combination of irinotecan silicasome nanoparticles with radiation therapy sensitizes immunotherapy by modulating the activation of the cGAS/STING pathway for colorectal cancer.Materials today. Bio · 2023Article
- Adaptation of the Tumor Antigen Presentation Machinery to Ionizing Radiation.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Review
- NOD-like Receptors-Emerging Links to Obesity and Associated Morbidities.International journal of molecular sciences · 2023Review
- NLRC5-CIITA Fusion Protein as an Effective Inducer of MHC-I Expression and Antitumor Immunity.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancers can escape immunesurveillance by diminishing the expression of MHC class-I molecules (MHC-I) and components of the antigen-processing machinery (APM). Developing new approaches to reverse these defects could boost the efforts to restore antitumor immunity. Recent studies have shown that the expression of MHC-I and antigen-processing molecules is transcriptionally regulated by NOD-like receptor CARD domain containing 5 (NLRC5). To investigate whether NLRC5 could be used to improve tumor immunogenicity, we established stable lines of B16-F10 melanoma cells expressing NLRC5 (B16-5), the T cell co-stimulatory molecule CD80 (B16-CD80) or both (B16-5/80). Cells harboring NLRC5 constitutively expressed MHC-I and LMP2, LMP7 and TAP1 genes of the APM. The B16-5 cells efficiently presented the melanoma antigenic peptide gp10025-33 to Pmel-1 TCR transgenic CD8(+) T cells and induced their proliferation. In the presence of CD80, B16-5 cells stimulated Pmel-1 cells even without the addition of gp100 peptide, indicating that NLRC5 facilitated the processing and presentation of endogenous tumor antigen. Upon subcutaneous implantation, B16-5 cells showed markedly reduced tumor growth in C57BL/6 hosts but not in immunodeficient hosts, indicating that the NLRC5-expressing tumor cells elicited antitumor immunity. Following intravenous injection, B16-5 and B16-5/80 cells formed fewer lung tumor foci compared to control cells. In mice depleted of CD8(+) T cells, B16-5 cells formed large subcutaneous and lung tumors. Finally, immunization with irradiated B16-5 cells conferred protection against challenge by parental B16 cells. Collectively, our findings indicate that NLRC5 could be exploited to restore tumor immunogenicity and to stimulate protective antitumor immunity.
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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.