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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Interleukin 36, alpha

IL-1F6, interleukin-1 family, member-6, FIL1epsilon
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Top mentioned proteins: IL-1beta, IL-1F9, IL-1ra, IL-1Rrp2, IL1F10
Papers on IL-1F6
IL-36 promotes myeloid cell infiltration, activation, and inflammatory activity in skin.
Johnston et al., Ann Arbor, United States. In J Immunol, 2014
The IL-1 family members IL-36α (IL-1F6), IL-36β (IL-1F8), and IL-36γ (IL-1F9) and the receptor antagonist IL-36Ra (IL-1F5) constitute a novel signaling system that is poorly understood.
Decreased expression of interleukin-36α predicts poor prognosis in colorectal cancer patients.
Chen et al., Shanghai, China. In Int J Clin Exp Pathol, 2013
Interleukin-36α (IL-36α), previously designated as IL-1F6, has been found to have a pathogenic role in psoriasis.
Alterations of plasma inflammatory biomarkers in the healthy and chronic obstructive pulmonary disease patients with or without acute exacerbation.
Wang et al., Shanghai, China. In J Proteomics, 2012
20 mediators were significantly different between 3 groups (p<0.05), of which, Cerberus 1, Growth Hormone R, IL-1F6, IL-17B R, IL-17D, IL-19, Lymphotoxin beta, MMP-10, Thrombopoietin and TLR4 were correlated with DESS scores (p<0.05).
The double-stranded RNA analogue polyinosinic-polycytidylic acid induces keratinocyte pyroptosis and release of IL-36γ.
Jensen et al., Philadelphia, United States. In J Invest Dermatol, 2012
IL-36 is the common name for the three IL-1 family members IL-36α, IL-36β, and IL-36γ, formerly known as IL-1F6, IL-1F8, and IL-1F9, respectively.
Interleukin-36 (IL-36) ligands require processing for full agonist (IL-36α, IL-36β, and IL-36γ) or antagonist (IL-36Ra) activity.
Sims et al., Seattle, United States. In J Biol Chem, 2012
Interleukin-36 (IL-36) ligands require processing for full agonist (IL-36alpha, IL-36beta, and IL-36gamma) or antagonist (IL-36Ra) activity
IL-36α exerts pro-inflammatory effects in the lungs of mice.
LeVine et al., Boston, United States. In Plos One, 2011
The current study sought to investigate the effects of IL-36α (IL-1F6) and test the hypothesis that IL-36α acts as a pro-inflammatory cytokine in the lung in vivo.
IL-36R ligands are potent regulators of dendritic and T cells.
Gabay et al., Genève, Switzerland. In Blood, 2011
A critical role of IL-36R ligands in the interface between innate and adaptive immunity, leading to the stimulation of T helper responses.
Engagement of IL-1 receptor accessory protein (IL-1RAcP) with the monoclonal antibody AY19 provides co-activating signals and prolongs the CD2-induced proliferation of peripheral blood lymphocytes.
Marie-Cardine et al., Paris, France. In Immunol Lett, 2011
IL-1 receptor accessory protein (IL-1RAcP) is the second subunit required to form a functional receptor complex for IL-1α and β, IL-1F6, IL-1F8, IL1-F9 and IL-33.
Regulation and function of the IL-1 family cytokine IL-1F9 in human bronchial epithelial cells.
Kato et al., Chicago, United States. In Am J Respir Cell Mol Biol, 2011
Messenger (m)RNAs for IL-1F6 and IL-1F9, but not IL-1F5, IL-1F8 or IL-1F10, were significantly up-regulated by TNF, IL-1β, IL-17 and the Toll-like receptor (TLR)3 ligand double-stranded (ds)RNA.
Expression of interleukin (IL)-1 family members upon stimulation with IL-17 differs in keratinocytes derived from patients with psoriasis and healthy donors.
Wittmann et al., Hannover, Germany. In Br J Dermatol, 2011
RESULTS: In the presence of IL-17, psoriasis-derived keratinocytes showed a significantly higher induction of the proinflammatory IL-1 family members IL-1F6 and IL-1F9, but not of anti-inflammatory members IL-1F5, IL-1F7 or IL-1F3 compared with keratinocytes from healthy individuals.
IL-1F5, -F6, -F8, and -F9: a novel IL-1 family signaling system that is active in psoriasis and promotes keratinocyte antimicrobial peptide expression.
Gudjonsson et al., Ann Arbor, United States. In J Immunol, 2011
Transcripts for IL-1F5, -1F6, -1F8, and -1F9 are all significantly increased in the involved skin of bitransgenic mice compared with their monotransgenic controls.
Quantitative and qualitative urinary cellular patterns correlate with progression of murine glomerulonephritis.
Kon et al., Sapporo, Japan. In Plos One, 2010
Cells immunopositive for Wilms tumor 1 (podocyte marker) and interleukin-1 family, member 6 (damaged DT and CD marker) in the kidney significantly decreased and increased in BXSB versus B6, respectively.
IL-1RL2 and its ligands contribute to the cytokine network in psoriasis.
Sims et al., Seattle, United States. In J Immunol, 2010
In this article, we show that treatment of mouse skin overexpressing the IL-1 family member, IL-1F6, with phorbol ester leads to an inflammatory condition with macroscopic and histological similarities to human psoriasis.
Local overexpression of interleukin-1 family, member 6 relates to the development of tubulointerstitial lesions.
Kon et al., Japan. In Lab Invest, 2010
local overexpression related to the development of tubulointerstitial lesions
Externalization of the leaderless cytokine IL-1F6 occurs in response to lipopolysaccharide/ATP activation of transduced bone marrow macrophages.
Gabel et al., Seattle, United States. In J Immunol, 2009
IL-1F6 can be externalized via a stimulus-coupled mechanism comparable to that used by IL-1beta
The interleukin-1 receptor/Toll-like receptor superfamily: 10 years of progress.
O'Neill, Dublin, Ireland. In Immunol Rev, 2008
We now know a great deal more about this superfamily, with the description of novel IL-1 family members such as IL-1F6 signaling via IL-1Rrp2 and IL33 signaling via ST2.
The expanding family of interleukin-1 cytokines and their role in destructive inflammatory disorders.
Taylor et al., Newcastle upon Tyne, United Kingdom. In Clin Exp Immunol, 2007
IL-1F6, IL-1F8 and Il-1F9 are agonists and, along with their receptor IL-1Rrp2, are highly expressed in epithelial cells suggesting a role in immune defence in the skin and the gastrointestinal (GI) tract including the mouth.
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