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data indicate that IL-36gamma may participate as a key player in host defense mechanisms against invading pathogens in the female reproductive tract.
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The results presented here confirm that IL-36gamma is a robust, specific, and reliable biomarker for psoriatic inflammation that outperforms previously reported biomarkers and is likely to withstand all challenges in real-life primary and secondary dermatologic care.
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Polymorphisms in IL36G gene are associated with plaque psoriasis. IL36G has previously demonstrated markedly increased levels in plaque psoriasis patients and is linked to IL-23/IL-17 axis critical in psoriasis pathology.
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Increased production and activation of IL-36gamma may act on neutrophils and further exaggerate neutrophilic inflammation in CRS.
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this study not only advances our understanding of how IL-36 cytokines may control mucosal inflammation, but also establishes EGFR signaling as a potentially important modulator of IL-36 cytokine function
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The expression of IL-36gamma by oral epithelial cells in response to P. gingivalis might enable the subsequent autocrine stimulation of PGLYRP2 expression. Our data identify how IL-36gamma may promote oral mucosal homeostasis by regulating PGLYRP2 expression.
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Interleukin 36 gamma (IL-36gamma) is detected in the immune and vascular compartments in the tumor microenvironment.
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serum IL-36gamma levels were higher in active systemic lupus erythematosus patients and correlated with disease activity and arthritis
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Cathepsin S was identified as the major IL-36gamma-activating protease expressed in epithelial cells.
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enhanced expression of IL-36gamma was observed in plasma and bronchoalveolar lavage fluid of patients with acute respiratory distress syndrome because of bacterial pneumonia
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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.
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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]
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IL-36gamma inhibits differentiation and induces inflammation of keratinocyte via Wnt signaling pathway in psoriasis.
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IL-36gamma-stimulated endothelial cells secrete the proinflammatory chemokines IL-8, CCL2 and CCL20.
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skin injury increases IL-36gamma via the activation of TLR3-SLUG-VDR axis and IL-36gamma induces REG3A to promote wound healing
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Autocrine and Paracrine Regulation of Keratinocyte Proliferation through a Novel Nrf2-IL-36gamma Pathway
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Here the authors show that Mycobacterium tuberculosis infection of macrophages induces IL-36gamma production in a 2-stage-regulated fashion.
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IL-36gamma, a member of the IL-1 superfamily, is involved in host defense and contributes to proinflammatory responses and development of inflammatory diseases.
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IL-36gamma is significantly more strongly expressed in the epidermis of patients with psoriasis-based erythroderma than in other inflammatory skin diseases.
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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.