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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.
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IRF6 is likely to promote inflammation to P. gingivalis through its regulation of IL-36gamma.
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Findings indicate that Interleukin (IL)-1beta-induced interleukin 36 gamma (IL-36gamma) expression is mediated by the activation of transcriptional factors, NF-kappaB p65 and AP-1 (c-jun).
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IL36G was identified as strong regulators of skin pathology in both lesional and non-lesional skin samples.
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Decreased Langerhans cell responses to IL36G: altered innate immunity in patients with recurrent respiratory papillomatosis
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IL-36gamma expression inversely correlated with the progression of human melanoma and lung cancer.
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IL-36gamma is a valuable biomarker in psoriasis patients, both for diagnostic purposes and measurement of disease activity during the clinical course
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CAMP induces IL-36gamma expression leading to initiation of skin inflammation and occasional exacerbations of psoriasis.
