ArticleFrontiers in microbiology2016
IL-36γ Augments Host Defense and Immune Responses in Human Female Reproductive Tract Epithelial Cells.
Article in Frontiers in microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed.
- FloxedCells · 2024Article
- The Interplay betweenMicroorganisms · 2023Review
- Interleukin-36γ is causative for liver damage upon infection with Rift Valley fever virus in type I interferon receptor-deficient mice.Frontiers in immunology · 2023Article
- Immunometabolic and potential tumor-promoting changes in 3D cervical cell models infected with bacterial vaginosis-associated bacteria.Communications biology · 2022Article
- IL-36 in chronic inflammation and fibrosis - bridging the gap?The Journal of clinical investigation · 2021Review
- Interleukin-36 Cytokines in Infectious and Non-Infectious Lung Diseases.Frontiers in immunology · 2021Review
- The Role of IL-36 in Infectious Diseases: Potential Target for COVID-19?Frontiers in immunology · 2021Review
- Role of IL-36 Cytokines in the Regulation of Angiogenesis Potential of Trophoblast Cells.International journal of molecular sciences · 2020Article
- 3D Oral and Cervical Tissue Models for Studying Papillomavirus Host-Pathogen Interactions.Current protocols in microbiology · 2020Article
- Hidradenitis suppurativa.Nature reviews. Disease primers · 2020Review
- Interleukin-36γ Is Elevated in Cervicovaginal Epithelial Cells in Women With Bacterial Vaginosis and In Vitro After Infection With Microbes Associated With Bacterial Vaginosis.The Journal of infectious diseases · 2020Article
- New Insights inFrontiers in cellular and infection microbiology · 2020Review
- IL-36γ Is a Key Regulator of Neutrophil Infiltration in the Vaginal Microenvironment and Limits Neuroinvasion in Genital HSV-2 Infection.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Article
- IL-36 Cytokines: Regulators of Inflammatory Responses and Their Emerging Role in Immunology of Reproduction.International journal of molecular sciences · 2019Review
- Interleukin-36 in Infectious and Inflammatory Skin Diseases.Frontiers in immunology · 2019Review
- IL-36γ induces a transient HSV-2 resistant environment that protects against genital disease and pathogenesis.Cytokine · 2018Article
- IL-36 and IL-1/IL-17 Drive Immunity to Oral Candidiasis via Parallel Mechanisms.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Linking cervicovaginal immune signatures, HPV and microbiota composition in cervical carcinogenesis in non-Hispanic and Hispanic women.Scientific reports · 2018Article
- Uterine Microbiota: Residents, Tourists, or Invaders?Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
IL-36γ is a proinflamatory cytokine which belongs to the IL-1 family of cytokines. It is expressed in the skin and by epithelial cells (ECs) lining lung and gut tissue. We used human 3-D organotypic cells, that recapitulate either in vivo human vaginal or cervical tissue, to explore the possible role of IL-36γ in host defense against pathogens in the human female reproductive tract (FRT). EC were exposed to compounds derived from virus or bacterial sources and induction and regulation of IL-36γ and its receptor was determined. Polyinosinic-polycytidylic acid (poly I:C), flagellin, and synthetic lipoprotein (FSL-1) significantly induced expression of IL-36γ in a dose-dependent manner, and appeared to be TLR-dependent. Recombinant IL-36γ treatment resulted in self-amplification of IL-36γ and its receptor (IL-36R) via increased gene expression, and promoted other inflammatory signaling pathways. This is the first report to demonstrate that the IL-36 receptor and IL-36γ are present in the human FRT EC and that they are differentially induced by microbial products at this site. We conclude that IL-36γ is a driver for epithelial and immune activation following microbial insult and, as such, may play a critical role in host defense in the FRT.
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Registered trials
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