ArticleScientific reports2015
STAT1 deficiency redirects IFN signalling toward suppression of TLR response through a feedback activation of STAT3.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 56 citations in OpenAlex.
- IFN-γ-Associated Signaling Networks in Interstitial Lung Disease Associated With Sjögren's Disease.Immunity, inflammation and disease · 2026Review
- Article
- ROS-Driven STAT1 S-Glutathionylation Sustains IFNγ Signaling and Pro-Inflammatory Microglial Polarization.Antioxidants (Basel, Switzerland) · 2025Article
- GDP-bound Rab37 modulates M2-like tumor-associated macrophage polarization by attenuating STAT1 translocation to downregulate the type I IFN pathway.British journal of cancer · 2025Article
- Role of TLRs as signaling cascades to combat infectious diseases: a review.Cellular and molecular life sciences : CMLS · 2025Review
- Modulation of esophageal squamous cell carcinoma progression: the impact of CCR7 on JAK2/STAT3 signaling pathway.Discover oncology · 2024Article
- Divergent Processing of Cell Stress Signals as the Basis of Cancer Progression: Licensing NFκB on Chromatin.International journal of molecular sciences · 2024Review
- Impaired autophagy in myeloid cells aggravates psoriasis-like skin inflammation through the IL-1β/CXCL2/neutrophil axis.Cell & bioscience · 2024Article
- STAT1-Deficient HPV E6/E7-Associated Cancers Maintain Host Immunocompetency against Therapeutic Intervention.Vaccines · 2024Article
- Inhibition of pro-inflammatory signaling in human primary macrophages by enhancing arginase-2 via target site blockers.Molecular therapy. Nucleic acids · 2023Article
- Regulation of intrinsic and extrinsic metabolic pathways in tumour-associated macrophages.The FEBS journal · 2023Review
- The Identification of Blood Biomarkers of Chronic Neuropathic Pain by Comparative Transcriptomics.Neuromolecular medicine · 2022Article
- Sweet taste receptor agonists attenuate macrophage IL-1β expression and eosinophilic inflammation linked to autophagy deficiency in myeloid cells.Clinical and translational medicine · 2022Article
- Glucosamine regulates macrophage function in heart failure.Clinical and translational medicine · 2022Article
- Nrf2-mediated anti-inflammatory polarization of macrophages as therapeutic targets for osteoarthritis.Frontiers in immunology · 2022Review
- STAT1 coordinates intestinal epithelial cell death during gastrointestinal infection upstream of Caspase-8.Mucosal immunology · 2022Article
- High Interferon Signature Leads to Increased STAT1/3/5 Phosphorylation in PBMCs From SLE Patients by Single Cell Mass Cytometry.Frontiers in immunology · 2022Article
- Cyclic Attractors Are Critical for Macrophage Differentiation, Heterogeneity, and Plasticity.Frontiers in molecular biosciences · 2022Article
- PDLIM2 is highly expressed in Breast Cancer tumour-associated macrophages and is required for M2 macrophage polarization.Frontiers in oncology · 2022Article
- Monogenic autoimmunity and infectious diseases: the double-edged sword of immune dysregulation.Current opinion in immunology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interferons (IFNs) potentiate macrophage activation typically via a STAT1-dependent pathway. Recent studies suggest a functioning of STAT1-independent pathway in the regulation of gene expression by IFN-γ, thus pointing to the diversity in cellular responses to IFNs. Many functions of IFNs rely on cross-regulation of the responses to exogenous inflammatory mediators such as TLR ligands. Here we investigated the contribution of STAT1-independent pathway to macrophage activation and its underlying mechanism in the context of combined stimulation of IFN and TLR. We found that TLR-induced production of inflammatory cytokines (TNF-α, IL-12) was not simply nullified but was significantly suppressed by signaling common to IFN-γ and IFN-β in STAT1-null macrophages. Such a shift in the suppression of TLR response correlated with a sustained STAT3 activation and attenuation of NF-κB signaling. Using a JAK2/STAT3 pathway inhibitor or STAT3-specific siRNA, blocking STAT3 in that context restored TNF-α production and NF-κB signaling, thus indicating a functional cross-regulation among STAT1, STAT3, and NF-κB. Our results suggest that STAT1 deficiency reprograms IFN signaling from priming toward suppression of TLR response via feedback regulation of STAT3, which may provide a new insight into the host defense response against microbial pathogens in a situation of STAT1 deficiency.
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