ArticleJournal of neuroinflammation2015
Interleukin-36γ is expressed by neutrophils and can activate microglia, but has no role in experimental autoimmune encephalomyelitis.
Article in Journal of neuroinflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Neutrophil to lymphocyte ratio and platelet to lymphocyte ratio as prognostic predictors for delirium in critically ill patients: a systematic review and meta-analysis.BMC anesthesiology · 2023Pooled it
- Calprotectin as a Biomarker for Infectious Diseases: A Comparative Review with Conventional Inflammatory Markers.International journal of molecular sciences · 2025Review
- High level of systemic immune inflammation index elevates delirium risk among patients in intensive care unit.Scientific reports · 2024Article
- Neurovascular unit, neuroinflammation and neurodegeneration markers in brain disorders.Frontiers in cellular neuroscience · 2024Review
- The Protective Role of IL-36/IL-36R Signal in Con A-Induced Acute Hepatitis.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- IL-36 Cytokines: Their Roles in Asthma and Potential as a Therapeutic.Frontiers in immunology · 2022Review
- Interleukin-36: Structure, Signaling and Function.Advances in experimental medicine and biology · 2021Review
- The Role of IL-36 in Infectious Diseases: Potential Target for COVID-19?Frontiers in immunology · 2021Review
- Increased serum IL-36β and IL-36γ levels in patients with neuromyelitis optica spectrum disorders: association with disease activity.BMC neurology · 2019Article
- Review
- Interleukin (IL)-33 and the IL-1 Family of Cytokines-Regulators of Inflammation and Tissue Homeostasis.Cold Spring Harbor perspectives in biology · 2019Review
- IL-1 Family Members Mediate Cell Death, Inflammation and Angiogenesis in Retinal Degenerative Diseases.Frontiers in immunology · 2019Review
- IL-36γ Protects against Severe Influenza Infection by Promoting Lung Alveolar Macrophage Survival and Limiting Viral Replication.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- ICAM1+ neutrophils promote chronic inflammation via ASPRV1 in B cell-dependent autoimmune encephalomyelitis.JCI insight · 2017Article
- Interleukin-36γ and IL-36 receptor signaling mediate impaired host immunity and lung injury in cytotoxic Pseudomonas aeruginosa pulmonary infection: Role of prostaglandin E2.PLoS pathogens · 2017Article
- Interleukin-36β provides protection against HSV-1 infection, but does not modulate initiation of adaptive immune responses.Scientific reports · 2017Article
- IL-36 receptor deletion attenuates lung injury and decreases mortality in murine influenza pneumonia.Mucosal immunology · 2017Article
- Human amnion epithelial cells rescue cell death via immunomodulation of microglia in a mouse model of perinatal brain injury.Stem cell research & therapy · 2017Article
- Pharmacological Stimulation of Phagocytosis Enhances Amyloid Plaque Clearance; Evidence from a Transgenic Mouse Model of ATTR Neuropathy.Frontiers in molecular neuroscience · 2017Article
- Imiquimod Treatment Causes Systemic Disease in Mice Resembling Generalized Pustular Psoriasis in an IL-1 and IL-36 Dependent Manner.Mediators of inflammation · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundExperimental autoimmune encephalomyelitis (EAE) is a model of inflammatory demyelinating diseases mediated by different types of leukocytes. How these cells communicate with each other to orchestrate autoimmune attacks is not fully understood, especially in the case of neutrophils, whose importance in EAE is newly established. The present study aimed to determine the expression pattern and role of different components of the IL-36 signaling pathway (IL-36α, IL-36β, IL-36γ, IL-36R) in EAE.
methodsEAE was induced by either active immunization with myelin peptide, passive transfer of myelin-reactive T cells or injection of pertussis toxin to transgenic 2D2 mice. The molecules of interest were analyzed using a combination of techniques, including quantitative real-time PCR (qRT-PCR), flow cytometry, Western blotting, in situ hybridization, and immunohistochemistry. Microglial cultures were treated with recombinant IL-36γ and analyzed using DNA microarrays. Different mouse strains were subjected to clinical evaluation and flow cytometric analysis in order to compare their susceptibility to EAE.
resultsOur observations indicate that both IL-36γ and IL-36R are strongly upregulated in nervous and hematopoietic tissues in different forms of EAE. IL-36γ is specifically expressed by neutrophils, while IL-36R is expressed by different immune cells, including microglia and other myeloid cells. In culture, microglia respond to recombinant IL-36γ by expressing molecules involved in neutrophil recruitment, such as Csf3, IL-1β, and Cxcl2. However, mice deficient in either IL-36γ or IL-36R develop similar clinical and histopathological signs of EAE compared to wild-type controls.
conclusionThis study identifies IL-36γ as a neutrophil-related cytokine that can potentially activate microglia, but that is only correlative and not contributory in EAE.
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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.