ArticleInflammation2014
NLRC5 mediates cytokine secretion in RAW264.7 macrophages and modulated by the JAK2/STAT3 pathway.
Article in Inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- ω-3 PUFAs Attenuate Postoperative Ileus by Modulating Macrophage Polarization via the JAK2/STAT3 Signaling Pathway.Journal of inflammation research · 2026Article
- Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.Cancer biology & therapy · 2025Article
- Pattern recognition receptors: function, regulation and therapeutic potential.Signal transduction and targeted therapy · 2025Review
- Nucleotide-binding oligomerization domain-like receptor family caspase recruitment domain containing protein 5 affects the progression of periodontitis by regulating the function of periodontal membrane cells.Journal of dental sciences · 2025Article
- Adaptor molecules mediate negative regulation of macrophage inflammatory pathways: a closer look.Frontiers in immunology · 2024Review
- NLRC5 affects diet-induced adiposity in female mice and co-regulates peroxisome proliferator-activated receptor PPARγ target genes.iScience · 2023Article
- NOD-like receptor NLRC5 promotes neuroinflammation and inhibits neuronal survival in Parkinson's disease models.Journal of neuroinflammation · 2023Article
- HSP27 modulates tumoural immune evasion by enhancing STAT3-mediated upregulation of PD-L1 and NLRC5 in ovarian cancer.Ecancermedicalscience · 2023Article
- Teleost NOD-like receptors and their downstream signaling pathways: A brief review.Fish and shellfish immunology reports · 2022Review
- Review
- NLRC5 Deficiency Deregulates Hepatic Inflammatory Response but Does Not Aggravate Carbon Tetrachloride-Induced Liver Fibrosis.Frontiers in immunology · 2021Article
- NLRC5: A Potential Target for Central Nervous System Disorders.Frontiers in immunology · 2021Review
- NLRC5 Serves as a Pro-viral Factor During Influenza Virus Infection in Chicken Macrophages.Frontiers in cellular and infection microbiology · 2020Article
- Article
- NLRC5 inhibits neointima formation following vascular injury and directly interacts with PPARγ.Nature communications · 2019Article
- Emerging Roles for NLRC5 in Immune Diseases.Frontiers in pharmacology · 2019Review
- NLRC5 Functions beyond MHC I Regulation-What Do We Know So Far?Frontiers in immunology · 2017Review
- NLRC5 Mediates IL-6 and IL-1β Secretion in LX-2 Cells and Modulated by the NF-κB/Smad3 Pathway.Inflammation · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nucleotide-binding domain leucine-rich repeat proteins (NLRs), a class of innate immune receptors that respond to pathogen attack or cellular stress, have gained increasing attention. NLRC5 is the largest member of NLR family, which has recently been identified as a critical regulator of immune responses. In this study, we explore the role of NLRC5 in cytokine secretion and the role of the JAK2/STAT3 signaling pathway in lipopolysaccharide-induced NLRC5 expression in RAW264.7 cells. We demonstrated that overexpression of NLRC5 results in a downregulation of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) secretion; on the other hand, knockdown of NLRC5 by transfecting siRNA enhanced IL-6 and TNF-α secretion in RAW264.7 cells. These results indicated that NLRC5 plays a negative role in the regulation of IL-6 and TNF-α. Meanwhile, AG490 (a specific inhibitor of the JAK2/STAT3 signaling pathway) and JAK2 siRNA were used to manipulate JAK2/STAT3 activity. Finally, the results showed that AG490 and JAK2 siRNA inhibited NLRC5 expression and the expression levels of p-JAK2 and p-STAT3. We, for the first time, demonstrate that the inhibition of the JAK2/STAT3 signaling pathway results in decrease of NLRC5 expression.
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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.