ArticleImmunologic research2015
Poly(I:C) induces controlled release of IL-36γ from keratinocytes in the absence of cell death.
Article in Immunologic research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- Unveiling exosomes: Cutting-edge isolation techniques and their therapeutic potential.Journal of cellular and molecular medicine · 2024Review
- Exosome-Mediated Antigen Delivery: Unveiling Novel Strategies in Viral Infection Control and Vaccine Design.Vaccines · 2024Review
- Small extracellular vesicles as key players in cancer development caused by human oncogenic viruses.Infectious agents and cancer · 2022Review
- MES SV40 Cells Are Sensitive to Lipopolysaccharide, Peptidoglycan, and Poly I:C Expressing IL-36 Cytokines.International journal of molecular sciences · 2022Article
- Epithelial cells release IL-36α in extracellular vesicles following mechanical damage.Biochemical and biophysical research communications · 2022Article
- Exosome Processing and Characterization Approaches for Research and Technology Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Review
- Extracellular vesicles produced by primary human keratinocytes in response to TLR agonists induce stimulus-specific responses in antigen-presenting cells.Cellular signalling · 2021Article
- The Role of IL-36 in Infectious Diseases: Potential Target for COVID-19?Frontiers in immunology · 2021Review
- Co-Isolation of Cytokines and Exosomes: Implications for Immunomodulation Studies.Frontiers in immunology · 2021Review
- Role of IL-36 Cytokines in the Regulation of Angiogenesis Potential of Trophoblast Cells.International journal of molecular sciences · 2020Article
- Human Papillomavirus and carcinogenesis: Novel mechanisms of cell communication involving extracellular vesicles.Cytokine & growth factor reviews · 2020Review
- Pathogenic role of exosomes and microRNAs in HPV-mediated inflammation and cervical cancer: A review.International journal of cancer · 2020Review
- Modulating Cytokine Production via Select Packaging and Secretion From Extracellular Vesicles.Frontiers in immunology · 2020Review
- Autophagy Suppresses Toll-Like Receptor 3-Mediated Inflammatory Reaction in Human Epidermal Keratinocytes.BioMed research international · 2020Article
- Enhanced Wound Healing- and Inflammasome-Associated Gene Expression in TNFAIP3-Interacting Protein 1- (TNIP1-) Deficient HaCaT Keratinocytes Parallels Reduced Reepithelialization.Mediators of inflammation · 2020Article
- Altered Monocyte and Langerhans Cell Innate Immunity in Patients With Recurrent Respiratory Papillomatosis (RRP).Frontiers in immunology · 2020Article
- Inhibition of Poly(I:C)-Induced Inflammation by Salvianolic Acid A in Skin Keratinocytes.Annals of dermatology · 2019Article
- IL-36 Cytokines: Regulators of Inflammatory Responses and Their Emerging Role in Immunology of Reproduction.International journal of molecular sciences · 2019Review
- IL-36γ induces a transient HSV-2 resistant environment that protects against genital disease and pathogenesis.Cytokine · 2018Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
The epithelium is part of an integrated immune system where cytokines, toll-like receptors and their ligands, and extracellular vesicles play a crucial role in initiating an innate immune response. IL-36γ is a pro-inflammatory member of the IL-1 family that is mainly expressed by epithelial cells, but regulation of its expression and release are only beginning to be understood. Previous studies reported that IL-36γ is abundant in recurrent respiratory papillomatosis, a rare but devastating disease caused by human papillomaviruses (HPV) types 6 and 11, in which papillomas recurrently grow in and block the airway. Despite the overexpression of IL-36γ, papilloma tissues show no evidence of inflammation, possibly due to suppression of its release by HPVs. We have used primary human foreskin keratinocytes as a model to study IL-36γ regulation in normal epithelial cells. Low doses of poly(I:C) mediate expression and release of IL-36γ without inducing the cell death reported by those using high doses. PKR, an enzyme required for inflammasome activation, does not contribute to controlled release of IL36γ. The keratinocytes secrete IL-36γ in two forms, soluble and in extracellular vesicles. We conclude that there are two separately regulated pathways for the controlled secretion of IL-36γ from keratinocytes, which could contribute to the modulation of both local and systemic immune responses to viruses and other pathogens.
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