ArticleJournal of immunology (Baltimore, Md. : 1950)2014
Cellular stress amplifies TLR3/4-induced CXCL1/2 gene transcription in mononuclear phagocytes via RIPK1.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- RANKL inhibits macrophage proinflammatory Toll-like receptor 2 and 4 signaling and impairs killing of intracellular bacteria.ImmunoHorizons · 2026Article
- Bioactive compound C498-0670 alleviates LPS-induced sepsisFrontiers in immunology · 2023Article
- The HSP GRP94 interacts with macrophage intracellular complement C3 and impacts M2 profile during ER stress.Cell death & disease · 2021Article
- The C-X-C Motif Chemokine Ligand 1 Sustains Breast Cancer Stem Cell Self-Renewal and Promotes Tumor Progression and Immune Escape Programs.Frontiers in cell and developmental biology · 2021Article
- Diesel Exhaust Particulates Induce Neutrophilic Lung Inflammation by Modulating Endoplasmic Reticulum Stress-Mediated CXCL1/KC Expression in Alveolar Macrophages.Molecules (Basel, Switzerland) · 2020Article
- LACC1 Required for NOD2-Induced, ER Stress-Mediated Innate Immune Outcomes in Human Macrophages and LACC1 Risk Variants Modulate These Outcomes.Cell reports · 2019Article
- ER stress abrogates the immunosuppressive effect of IL-10 on human macrophages through inhibition of STAT3 activation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019Article
- TMEM203 is a binding partner and regulator of STING-mediated inflammatory signaling in macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Unfolded Protein Response Differentially Regulates TLR4-Induced Cytokine Expression in Distinct Macrophage Populations.Frontiers in immunology · 2019Article
- Necrostatin-1 Attenuates Trauma-Induced Mouse Osteoarthritis and IL-1β Induced Apoptosis via HMGB1/TLR4/SDF-1 in Primary Mouse Chondrocytes.Frontiers in pharmacology · 2018Article
- Endoplasmic reticulum stress cooperates with Toll-like receptor ligation in driving activation of rheumatoid arthritis fibroblast-like synoviocytes.Arthritis research & therapy · 2017Article
- Hyperglycemia Aggravates Hepatic Ischemia and Reperfusion Injury by Inhibiting Liver-Resident Macrophage M2 PolarizationFrontiers in immunology · 2017Article
- The unfolded protein response in immunity and inflammation.Nature reviews. Immunology · 2016Review
- TRPV4 Mechanosensitive Ion Channel Regulates Lipopolysaccharide-Stimulated Macrophage Phagocytosis.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Transcriptional regulation of myeloid-derived suppressor cells.Journal of leukocyte biology · 2015Review
- cEBP Homologous Protein Expression in Macrophages Regulates the Magnitude and Duration of IL-6 Expression and Dextran Sodium Sulfate Colitis.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The impact of environmental stressors on the magnitude of specific chemokine gene expression was examined in mouse bone marrow-derived macrophages stimulated through various TLRs. Levels of TLR-stimulated CXCL1 and CXCL2 but not CXCL10 or CCL5 mRNAs were selectively enhanced (>10-fold) in stressed macrophages. The amplification was also manifested for other proinflammatory cytokines, including TNF-α, IL-1α, and IL-6. Responses through TLR3 and TLR4 exhibited the greatest sensitivity, reflecting a requirement for Toll/IL-IR domain-containing adaptor-inducing IFN-β (TRIF), the adaptor protein selectively associated with these TLRs. IFN regulatory factor 3, a transcription factor that is downstream of TLR4/TRIF signaling, was not required for sensitivity to stress-induced chemokine amplification. c/EBP homologous protein and X box binding protein 1 have been reported to enhance inflammatory cytokine responses but are not required for amplification of TLR3/4-induced CXCL1 expression. Rather, receptor-interacting protein kinase 1, a kinase also linked with TLR3/4/TRIF signaling, is required and involves a stress-dependent increase in its abundance and ubiquitination. Whereas NF-κB activation is necessary for TLR-induced chemokine gene transcription, this factor does not appear to be the primary mechanistic target of environmental stress. The application of stress also enhanced chemokine expression in macrophages infiltrating the peritoneal cavity but was not observed in the resident peritoneal cells or in the liver. These findings identify novel mechanisms for modulating the magnitude and duration of selective TLR-induced chemokine and cytokine gene expression and further establish the importance of cell stress pathways in coordinating the outcomes of cellular and tissue injury.
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