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

Interleukin 36, gamma

IL-1F9, IL-1H1, IL-1RP2, IL-1 h, IL-1epsilon
The protein encoded by this gene is a member of the interleukin 1 cytokine family. The activity of this cytokine is mediated by interleukin 1 receptor-like 2 (IL1RL2/IL1R-rp2), and is specifically inhibited by interleukin 1 family, member 5 (IL1F5/IL-1 delta). Interferon-gamma, tumor necrosis factor-alpha and interleukin 1, beta (IL1B) are reported to stimulate the expression of this cytokine in keratinocytes. The expression of this cytokine in keratinocytes can also be induced by a contact hypersensitivity reaction or herpes simplex virus infection. This gene and eight other interleukin 1 family genes form a cytokine gene cluster on chromosome 2. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: IL-1beta, IL-1F6, IL-1ra, IL-1Rrp2, IL-18
Papers on IL-1F9
IL-36γ (IL-1F9) is a biomarker for psoriasis skin lesions.
New
Wenzel et al., Bonn, Germany. In J Invest Dermatol, Apr 2015
In recent years, different genes and proteins have been highlighted as potential biomarkers for psoriasis, one of the most common inflammatory skin diseases worldwide.
Brazilian Red Propolis Attenuates Inflammatory Signaling Cascade in LPS-Activated Macrophages.
Mayer et al., São Paulo, Brazil. In Plos One, 2014
BRP significantly reduced the up-regulation promoted by LPS of transcription of genes in inflammatory signaling (Pdk1, Pak1, Nfkb1, Mtcp1, Gsk3b, Fos and Elk1) and of Il1β and Il1f9 (fold-change rate > 5), which were further confirmed by the inhibition of NF-κB and MAPK signaling pathways.
Synergistic Proinflammatory Responses by IL-17A and Toll-Like Receptor 3 in Human Airway Epithelial Cells.
Suda et al., Hamamatsu, Japan. In Plos One, 2014
In this study, we demonstrated that IL-17A and polyI:C, the ligand of TLR3, synergistically induced the expression of proinflammatory cytokines and chemokines (G-CSF, IL-8, CXCL1, CXCL5, IL-1F9), but not type I interferon (IFN-α1, -β) in primary culture of normal human bronchial epithelial cells.
Genetic predisposition to calcific aortic stenosis and mitral annular calcification.
Review
Barbarash et al., Kemerovo, Russia. In Mol Biol Rep, 2014
A number of other polymorphisms, such as PvuII polymorphism within the ORα gene, rs1042636 polymorphism within the CaSR gene, rs3024491, rs3021094, rs1554286, and rs3024498 polymorphisms within the IL10 gene, rs662 polymorphism within the PON1 gene, rs2276288 polymorphism within the MYO7A gene, rs5194 polymorphism within the AGTR1 gene, rs2071307 polymorphism within the ELN gene, rs17659543 and rs13415097 polymorphisms within the IL1F9 gene may correlate with a risk of calcific valve stenosis with moderate level of evidence.
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.
Keratinocyte overexpression of IL-17C promotes psoriasiform skin inflammation.
Ward et al., Ann Arbor, United States. In J Immunol, 2013
ECs stimulated with IL-17C produce increased TNF-α and KCs stimulated with IL-17C/TNF-α produce similar inflammatory gene response patterns as those elicited by IL-17A/TNF-α, including increases in IL-17C, TNF-α, IL-8, IL-1α/β, IL-1F5, IL-1F9, IL-6, IL-19, CCL20, S100A7/A8/A9, DEFB4, lipocalin 2, and peptidase inhibitor 3 (p < 0.05), indicating a positive proinflammatory feedback loop between the epidermis and ECs.
Genetic associations with valvular calcification and aortic stenosis.
Impact
CHARGE Extracoronary Calcium Working Group et al., Montréal, Canada. In N Engl J Med, 2013
Two SNPs (rs17659543 and rs13415097) near the proinflammatory gene IL1F9 achieved genomewide significance for mitral annular calcification (P=1.5×10(-8) and P=1.8×10(-8), respectively), but the findings were not replicated consistently.
IL-36γ/IL-1F9, an innate T-bet target in myeloid cells.
Mühl et al., Frankfurt am Main, Germany. In J Biol Chem, 2013
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.
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.
Expression of IL-1Rrp2 by human myelomonocytic cells is unique to DCs and facilitates DC maturation by IL-1F8 and IL-1F9.
Foster et al., Nottingham, United Kingdom. In Eur J Immunol, 2012
We also show that IL-1F8 or IL-1F9 cytokines, which signal through IL-1Rrp2, induce maturation of MDDCs, as measured by increased expression of HLA-DR and CD83 and decreased expression of CD1a.
Interleukin-36 (IL-36) ligands require processing for full agonist (IL-36α, IL-36β, and IL-36γ) or antagonist (IL-36Ra) activity.
GeneRIF
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-36R ligands are potent regulators of dendritic and T cells.
GeneRIF
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.
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.
Regulation and function of the IL-1 family cytokine IL-1F9 in human bronchial epithelial cells.
GeneRIF
Kato et al., Chicago, United States. In Am J Respir Cell Mol Biol, 2011
Regulation and function of the IL-1 family cytokine IL-1F9 in human bronchial epithelial cells.
IL-1F5, -F6, -F8, and -F9: a novel IL-1 family signaling system that is active in psoriasis and promotes keratinocyte antimicrobial peptide expression.
GeneRIF
Gudjonsson et al., Ann Arbor, United States. In J Immunol, 2011
Expression of IL-1F9 is increased in human plaque psoriasis skin and is overexpressed in a transgenic mouse psoriasis model.
The expanding family of interleukin-1 cytokines and their role in destructive inflammatory disorders.
Review
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.
Transcriptional response of bronchial epithelial cells to Pseudomonas aeruginosa: identification of early mediators of host defense.
GeneRIF
Datson et al., Leiden, Netherlands. In Physiol Genomics, 2005
This report demonstrates expression of IL1F9 by bronchial epithelial cells induced by pro-inflammatory stimuli, suggesting a function of this molecule in airway inflammation.
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