ArticleThe Journal of biological chemistry2012
Regulation of class I major histocompatibility complex (MHC) by nucleotide-binding domain, leucine-rich repeat-containing (NLR) proteins.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.
- Epigenetic regulation of major histocompatibility complexes in gastrointestinal malignancies and the potential for clinical interception.Clinical epigenetics · 2024Pooled it
- EZH2 inhibition mitigates HIV immune evasion, reduces reservoir formation, and promotes skewing of CD8Cell reports · 2025Article
- Microbiota regulates neonatal disease tolerance to virus-evoked necrotizing enterocolitis by shaping the STAT1-NLRC5 axis in the intestinal epithelium.Cell host & microbe · 2024Article
- The NLR family of innate immune and cell death sensors.Immunity · 2024Review
- Targeted demethylation and activation ofProceedings of the National Academy of Sciences of the United States of America · 2024Article
- A Ménage à trois: NLRC5, immunity, and metabolism.Frontiers in immunology · 2024Review
- The NLR gene family: from discovery to present day.Nature reviews. Immunology · 2023Review
- Review
- NLRC5 affects diet-induced adiposity in female mice and co-regulates peroxisome proliferator-activated receptor PPARγ target genes.iScience · 2023Article
- Identification of Two Genetic Loci Associated with Leukopenia after Chemotherapy in Patients with Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Spotlight on TAP and its vital role in antigen presentation and cross-presentation.Molecular immunology · 2022Review
- Nod-like Receptors: Critical Intracellular Sensors for Host Protection and Cell Death in Microbial and Parasitic Infections.International journal of molecular sciences · 2021Review
- NLRC5 regulates expression of MHC-I and provides a target for anti-tumor immunity in transmissible cancers.Journal of cancer research and clinical oncology · 2021Article
- MHC Class I Deficiency in Solid Tumors and Therapeutic Strategies to Overcome It.International journal of molecular sciences · 2021Review
- Review
- The MHC Class-I Transactivator NLRC5: Implications to Cancer Immunology and Potential Applications to Cancer Immunotherapy.International journal of molecular sciences · 2021Review
- NLRC5/CITA expression correlates with efficient response to checkpoint blockade immunotherapy.Scientific reports · 2021Article
- NLRC5 promotes transcription ofiScience · 2021Article
- NLRC5: A Potential Target for Central Nervous System Disorders.Frontiers in immunology · 2021Review
- NLRC5 Deficiency Deregulates Hepatic Inflammatory Response but Does Not Aggravate Carbon Tetrachloride-Induced Liver Fibrosis.Frontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Most of the nucleotide-binding domain, leucine-rich repeat (NLR) proteins regulate responses to microbial and damage-associated products. Class II transactivator (CIITA) has a distinct function as the master regulator of class II major histocompatibility complex (MHC-II) transcription. Recently, human NLRC5 was found to regulate MHC-I in cell lines; however, a host of conflicting positive and negative functions has been attributed to this protein. To address the function of NLRC5 in a physiologic setting, we generated an Nlrc5(-/-) strain that contains a deletion in the exon that encodes the nucleotide-binding domain. We have not detected a role for this protein in cytokine induction by pathogen-associated molecular patterns and viruses. However, Nlrc5(-/-) cells showed a dramatic decrease of classical (H-2K) and nonclassical (Tla) MHC-I expression by T/B lymphocytes, natural killer (NK) cells, and myeloid-monocytic lineages. As a comparison, CIITA did not affect mouse MHC-I expression. Nlrc5(-/-) splenocytes and bone marrow-derived macrophages were able to up-regulate MHC-I in response to IFN-γ; however, the absolute levels of MHC-I expression were significantly lower than WT controls. Chromatin immunoprecipitation of IFN-γ-treated cells indicates that Nlrc5 reduced the silencing H3K27me3 histone modification, but did not affect the activating AcH3 modification on a MHC-I promoter. In summary, we conclude that Nlrc5 is important in the regulation of MHC-I expression by reducing H3K27me3 on MHC-I promoter and joins CIITA as an NLR subfamily that controls MHC gene transcription.
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Registered trials
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.