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TLR/CLR signaling-induced IL-36alpha plays an important role for the development of psoriasiform dermatitis by enhancing Th17-related cytokine/chemokine production in skin-resident cells via a local autoamplification loop.
IL-36alpha is involved in induction and/or activation of hapten-specific T-cell subsets in the sensitization phase of contact hypersensitivity, but not essential for induction of local inflammation in the elicitation phase.
The data identify a novel role for IL-36 signaling in colonic inflammation and indicate that the IL-36R pathway may represent a novel target for therapeutic intervention.
IL-1 and IL-36 have roles as inflammatory mediators in pustular psoriasis in a mouse model
IL-1alpha and IL-36alpha form a self-amplifying inflammatory loop in vivo that in patients with insufficient counter regulatory mechanisms may become hyper-engaged and/or chronic
An essential role of C/EBPbeta in the regulation of the Il36A gene via the proximal half-CRE*C/EBP element in response to inflammatory stimuli.
IL-36 promotes myeloid cell infiltration, activation, and inflammatory activity in skin
IL-36alpha acts as a pro-inflammatory cytokine in the lungs independent of both IL-1alpha and IL-1beta.
Interleukin-36 (IL-36) ligands require processing for full agonist (IL-36alpha, IL-36beta, and IL-36gamma) or antagonist (IL-36Ra) activity
A critical role of IL-36R ligands in the interface between innate and adaptive immunity, leading to the stimulation of T helper responses.
Transcripts for IL-1F5, -1F6, -1F8, and -1F9 are all significantly increased in the involved skin of bitransgenic mice compared with their monotransgenic controls.
local overexpression related to the development of tubulointerstitial lesions
IL-1F6 can be externalized via a stimulus-coupled mechanism comparable to that used by IL-1beta
The molecular analysis revealed strong cooperative effects of IL-17A and IL-36 cytokines in regulating target genes, which was dependent on the proteolytic activation of the latter. Together these findings suggest an amplification cycle that can be initiated by IL-17A, involving IL-36 cytokines and immune cell derived proteases and resulting in active IL-36 cytokines which synergize with IL-17A
PTX3 and IL36alpha serum levels are increased in systemic lupus erythematosus patients when compared to normal control subjects
The authors report that, in Mycobacterium tuberculosis-infected macrophages, IL-36 signaling modulates cholesterol biosynthesis and efflux via LXR.
serum IL-36alpha levels were higher in active systemic lupus erythematosus patients and correlated with disease activity and arthritis
IL-36-mediated IL-6 and CXCL8 production in human lung fibroblasts and bronchial epithelial cells may be involved in pulmonary inflammation especially caused by bacterial or viral infections.
With a focus on the skin as a target for microbial and viral invasion, the current knowledge of IL-36: IL-36alpha, IL-36beta and IL-36gamma, functions is reviewed. One physiological function of the IL-36smay be to counteract microbial immune evasion. [Review]
Data suggest that interleukin-36alpha (IL-36alpha) plays an important role in the pathophysiology of inflammation and fibrosis in the pancreas via an autocrine function.
IL-36a was displayed to be able to suppress the growth of epithelial ovarian cancer cells in our setting, which is suggestive of its druggable potential in curing the epithelial ovarian cancer and that upregulation of IL-36a was found to be capable of inhibiting the growth of epithelial ovarian cancer cells.
Increased Expression of Interleukin-36 is associated with Inflammatory Bowel Disease.
IL-36alpha acts as a pro-inflammatory cytokine at cartilage level, by increasing the expression of markers of inflammation and cartilage catabolism.
Study shows that plasma concentrations of IL-36alpha and IL-36gamma are overexpressed in active systemic lupus erythematosus patients and that IL-36alpha has a substantial pro-inflammatory effect through regulation of IL-6 and CXCL8 production.
increases maturation of monocyte-derived dendritic cells
IL36A-IL36R axis is modulated in patients with primary Sjogren's syndrome.
IL-36alpha was highly expressed in nearly half of all colorectal cancer patients. Low expression level of IL-36alpha correlated with larger tumor size and advanced cancer stage. Low expression of IL-36alpha resulted in a poor prognosis of colorectal cancer patients.
Results show that IL-36alpha expression may play a pivotal role in determining the prognosis of hepatocellular carcinoma (HCC).
The novel cytokine interleukin-36alpha is expressed in psoriatic and rheumatoid arthritis synovium.
Expression of IL-1F6 is increased in human plaque psoriasis skin and in the lesional skin of transgenic mice compared with monotransgenic littermates.
Function as an agonist of NF-kappa B activation through the orphan IL-1-receptor-related protein 2. Could constitute part of an independent signaling system analogous to interleukin-1 alpha (IL-1A), beta (IL-1B) receptor agonist and interleukin-1 receptor type I (IL-1R1), that is present in epithelial barriers and takes part in local inflammatory response.
interleukin 1 family, member 6
, interleukin-1 family member 6
, interleukin 1 family, member 6 (epsilon)
, interleukin 1 family, member 6 (epsilon)-like
, FIL1 epsilon
, IL-1 epsilon
, interleukin 1 family, member 9
, interleukin-1 epsilon
, interleukin-1 homolog 1
, interleukin-36 alpha
, IL-1F6 (FIL-1-epsilon)
, interleukin 1, epsilon