ArticleThe Journal of biological chemistry2012
IL-36γ/IL-1F9, an innate T-bet target in myeloid cells.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 57 citations in OpenAlex.
- Monocytes Expressing IL-36G Play a Crucial Role in Atopic Dermatitis.Journal of cellular and molecular medicine · 2025Article
- Clinical relevance and therapeutic potential of IL-38 in immune and non-immune-related disordersEuropean cytokine network · 2022Review
- Regulation of Interleukin-36γ/IL-36R Signaling Axis by PIN1 in Epithelial Cell Transformation and Breast Tumorigenesis.Cancers · 2022Article
- Increased Levels of Interleukin-36 in Obesity and Type 2 Diabetes Fuel Adipose Tissue Inflammation by Inducing Its Own Expression and Release by Adipocytes and Macrophages.Frontiers in immunology · 2022Article
- Analysis of Il36a induction by C/EBPβ via a half-CRE•C/EBP element in murine macrophages in dependence of its CpG methylation level.Genes and immunity · 2021Article
- Cytokine/Chemokine Release Patterns and Transcriptomic Profiles of LPS/IFNγ-Activated Human Macrophages Differentiated with Heat-KilledInternational journal of molecular sciences · 2021Article
- IL-36 cytokines and gut immunity.Immunology · 2021Review
- IkBζ is a Key Regulator of Tumour Necrosis Factor-a and Interleukin-17A-mediated Induction of Interleukin-36g in Human Keratinocytes.Acta dermato-venereologica · 2021Article
- IL36 is a critical upstream amplifier of neutrophilic lung inflammation in mice.Communications biology · 2021Article
- IL-36 Cytokines Promote Inflammation in the Lungs of Long-Term Smokers.American journal of respiratory cell and molecular biology · 2021Article
- Tertiary Lymphoid Structures in Cancer: The Double-Edged Sword Role in Antitumor Immunity and Potential Therapeutic Induction Strategies.Frontiers in immunology · 2021Review
- Interleukin-36 Cytokines in Infectious and Non-Infectious Lung Diseases.Frontiers in immunology · 2021Review
- Seven immune-related genes prognostic power and correlation with tumor-infiltrating immune cells in hepatocellular carcinoma.Cancer medicine · 2020Article
- IL-36 signaling in keratinocytes controls early IL-23 production in psoriasis-like dermatitis.Life science alliance · 2020Article
- IL-36γ drives skin toxicity induced by EGFR/MEK inhibition and commensal Cutibacterium acnes.The Journal of clinical investigation · 2020Article
- Nasal Pneumococcal Density Is Associated with Microaspiration and Heightened Human Alveolar Macrophage Responsiveness to Bacterial Pathogens.American journal of respiratory and critical care medicine · 2020Article
- IL36 Cooperates With Anti-CTLA-4 mAbs to Facilitate Antitumor Immune Responses.Frontiers in immunology · 2020Article
- IL-36 Signaling in the Tumor Microenvironment.Advances in experimental medicine and biology · 2020Review
- The Significance of IL-36 Hyperactivation and IL-36R Targeting in Psoriasis.International journal of molecular sciences · 2019Review
- IL-36 Cytokines: Regulators of Inflammatory Responses and Their Emerging Role in Immunology of Reproduction.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
By concerted action in dendritic (DC) and T cells, T-box expressed in T cells (T-bet, Tbx21) is pivotal for initiation and perpetuation of Th1 immunity. Identification of novel T-bet-regulated genes is crucial for further understanding the biology of this transcription factor. By combining siRNA technology with genome-wide mRNA expression analysis, we sought to identify new T-bet-regulated genes in predendritic KG1 cells activated by IL-18. One gene robustly dependent on T-bet was IL-36γ, a recently described novel IL-1 family member. Promoter analysis revealed a T-bet binding site that, along with a κB site, enables efficient IL-36γ induction. Using knock-out animals, IL-36γ reliance on T-bet was extended to murine DC. IL-36γ expression by human myeloid cells was confirmed using monocyte-derived DC and M1 macrophages. The latter model was employed to substantiate dependence of IL-36γ on endogenous T-bet in human primary cells. Ectopic expression of T-bet likewise mediated IL-36γ production in HaCaT keratinocytes that otherwise lack this transcription factor. Additional experiments furthermore revealed that mature IL-36γ has the capability to establish an inflammatory gene expression profile in human primary keratinocytes that displays enhanced mRNA levels for TNFα, CCL20, S100A7, inducible NOS, and IL-36γ itself. Data presented herein shed further light on involvement of T-bet in innate immunity and suggest that IL-36γ, besides IFNγ, may contribute to functions of this transcription factor in immunopathology.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.