ArticleFrontiers in cell and developmental biology2022
Synergistic Effects of Toll-Like Receptor 1/2 and Toll-Like Receptor 3 Signaling Triggering Interleukin 27 Gene Expression in Chikungunya Virus-Infected Macrophages.
Article in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Research progress on the role of host factors in Chikungunya virus infection and intervention strategies.Virulence · 2026Review
- Overview of Chikungunya Virus Pathogenesis, Genome Variation, Epidemiology, and Control.Virus research · 2026Review
- GM-CSF and M-CSF Driven Differentiation Differentially Regulates Chikungunya Virus Infection and Antiviral Responses in Human Monocyte-Derived Macrophages.bioRxiv : the preprint server for biology · 2026Article
- Article
- Innate immune sensing of alphavirus chikungunya: balancing antiviral defense and pathogenesis.Frontiers in immunology · 2026Review
- Monocyte Dynamics in Chikungunya Fever: Sustained Activation and Vascular-Coagulation Pathway Involvement.Viruses · 2025Article
- Early events in dengue virus infection inducing cytokine storm: The dynamic interplay of pattern-recognition receptors, inflammasome activation, and biphasic NF-κB and STAT1-dependent inflammatory responses in human mononuclear phagocytes.PLoS neglected tropical diseases · 2025Article
- Review
- Research status and future perspectives of IL‑27 in the treatment of stroke (Review).International journal of molecular medicine · 2025Review
- Acute Immunological Biomarkers for Predicting Chronic Rheumatologic Disease After Chikungunya Virus Infection.Tropical medicine and infectious disease · 2025Article
- Transcriptomic Analysis of Mayaro Virus-Infected Human Macrophages: Effects on Inflammatory and Antiviral Response.The American journal of tropical medicine and hygiene · 2025Article
- IL-27 effects on HIVFrontiers in virology (Lausanne, Switzerland) · 2025Article
- Rosmarinic acid-mediated downregulation of RIG-I and p62 in microglia confers resistance to Japanese encephalitis virus-induced inflammation.BMC veterinary research · 2024Article
- Decellularized Matrices for the Treatment of Tissue Defects: from Matrix Origin to Immunological Mechanisms.Biomolecules & therapeutics · 2024Review
- Article
- Chikungunya virus vaccine: a decade of progress solving epidemiological dilemma, emerging concepts, and immunological interventions.Frontiers in microbiology · 2024Review
- Interleukin 27, like interferons, activates JAK-STAT signaling and promotes pro-inflammatory and antiviral states that interfere with dengue and chikungunya viruses replication in human macrophages.Frontiers in immunology · 2024Article
- Review
- American-Asian- and African lineages of Zika virus induce differential pro-inflammatory and Interleukin 27-dependent antiviral responses in human monocytes.Virus research · 2023Article
- Dissection of the macrophage response towards infection by theFrontiers in cellular and infection microbiology · 2022Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chikungunya virus (CHIKV) is the etiological agent of chikungunya fever (CHIKF), a self-limiting disease characterized by myalgia and severe acute or chronic arthralgia. CHIKF is associated with immunopathology and high levels of pro-inflammatory factors. CHIKV is known to have a wide range of tropism in human cell types, including keratinocytes, fibroblasts, endothelial cells, monocytes, and macrophages. Previously, we reported that CHIKV-infected monocytes-derived macrophages (MDMs) express high levels of interleukin 27 (IL27), a heterodimeric cytokine consisting of IL27p28 and EBI3 subunits, that triggers JAK-STAT signaling and promotes pro-inflammatory and antiviral response, in interferon (IFN)-independent manner. Based on the transcriptomic analysis, we now report that induction of IL27-dependent pro-inflammatory and antiviral response in CHIKV-infected MDMs relies on two signaling pathways: an early signal dependent on recognition of CHIKV-PAMPs by TLR1/2-MyD88 to activate NF-κB-complex that induces the expression of EBI3 mRNA; and second signaling dependent on the recognition of intermediates of CHIKV replication (such as dsRNA) by TLR3-TRIF, to activate IRF1 and the induction of IL27p28 mRNA expression. Both signaling pathways were required to produce a functional IL27 protein involved in the induction of ISGs, including antiviral proteins, cytokines, CC- and CXC- chemokines in an IFN-independent manner in MDMs. Furthermore, we reported that activation of TLR4 by LPS, both in human MDMs and murine BMDM, results in the induction of both subunits of IL27 that trigger strong IL27-dependent pro-inflammatory and antiviral response independent of IFNs signaling. Our findings are a significant contribution to the understanding of molecular and cellular mechanisms of CHIKV infection.
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