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Inflammatory cell expression of IL-9 (zeige IL9 Proteine) and IL-17C were increased in chronic rhinosinusitis, particularly with allergy and asthma. These interleukins may contribute to the pathogenesis of chronic rhinosinusitis with nasal polyps as well as atopy and may serve as therapeutic targets for disease management
Helicobacter pylori infection was associated with a significant increase in IL-17C expression in gastric mucosa. The role of IL-17C in the pathogenesis of H. pylori-induced diseases remains to be determined.
Data indicate that epithelial IL-17C promotes neutrophilic inflammation in the tumor microenvironment and suggest that IL-17C links a pathologic microbiota, as present in COPD (zeige ARCN1 Proteine) patients, with enhanced tumor growth.
IL-17C is an essential epithelial cell-derived cytokine.
Our study provides evidence that Staphylococcus aureus activates NOD2 in keratinocytes, resulting in an increased expression of IL-17C, a mechanism that may be dysregulated in atopic dermatitis.
Interleukin-17C is present in the tissue around aseptic loosened implants.
IL-17C is involved in the innate immune response of respiratory epithelial cells and is suppressed by cigarette smoke.
Data suggest that activation of TLR5 (zeige TLR5 Proteine) upregulates IL17C expression in cells from intestinal mucosa and colonic adenocarcinoma; IL17C expression is upregulated in intestinal mucosa cells from patients with ulcerative colitis compared with normal cells.
Keratinocyte overexpression of IL-17C promotes psoriasiform skin inflammation.
In our pilot study, we discovered significant changes in methylation patterns of genes IL-7 (zeige IL7 Proteine), IL-13 (zeige IL13 Proteine), IL-17C and TYK2 (zeige TYK2 Proteine) between henodialysis patients and healthy subjects
IL-17C+IL-6 (zeige IL6 Proteine) knockout mice reveal that IL17C may have a role in psoriasis and skin inflammation, explaining why IL6 (zeige IL6 Proteine) blockade treatment may not be effective
IL-17C is a critical factor that potentiates inflammatory responses and causes host injury during fungal infection.
IL-17A (zeige IL17A Proteine)-mediated expression of epithelial IL-17C amplifies the release of chemokines by epithelial cells and thereby contributes to the recruitment of neutrophils and systemic inflammation during acute P. aeruginosa pneumonia.
Smooth muscle cell-derived IL-17C plays a proatherogenic role by supporting the recruitment of Il17a (zeige IL17A Proteine)-positive Th17 cells to atherosclerotic lesions.
IL-17C and IL-17RE (zeige IL17RE Proteine) are dispensable for immunity to candidiasis
IL-17C plays a critical role in maintaining mucosal barrier integrity; IL-17C deficiency renders mice more susceptible to mucosal barrier breakage and development of colitis.
IL-17C is an essential autocrine cytokine that regulates innate epithelial immune responses.
IL-17C-interleukin-17 receptor E (zeige IL17RE Proteine) induced the expression of a nuclear IkappaB family member, IkappaBzeta (zeige NFKBIZ Proteine), in Th17 cells to potentiate the Th17 cell response
Intranasal administration of adenovirus expressing IL-17 (zeige IL17A Proteine) results in bronchoalveolar lavage neutrophilia and Th1 (zeige HAND1 Proteine)-type inflammatory gene expression in the lung.
The protein encoded by this gene is a T cell-derived cytokine that shares the sequence similarity with IL17. This cytokine was reported to stimulate the release of tumor necrosis factor alpha and interleukin 1 beta from a monocytic cell line. The expression of this cytokine was found to be restricted to activated T cells.
, Interleukin 17-3
, cytokine CX2