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Inflammatory cell expression of IL-9 (show IL9 ELISA Kits) 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 (show ARCN1 ELISA Kits) patients, with enhanced tumor growth.
IL-17C is an essential epithelial cell-derived cytokine.
Our study provides evidence that Staphylococcus aureus activates NOD2 (show NOD2 ELISA Kits) 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 (show TLR5 ELISA Kits) 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 (show IL7 ELISA Kits), IL-13 (show IL13 ELISA Kits), IL-17C and TYK2 (show TYK2 ELISA Kits) between henodialysis patients and healthy subjects
IL-17C+IL-6 (show IL6 ELISA Kits) knockout mice reveal that IL17C may have a role in psoriasis and skin inflammation, explaining why IL6 (show IL6 ELISA Kits) 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 (show IL17A ELISA Kits)-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 (show IL17A ELISA Kits)-positive Th17 cells to atherosclerotic lesions.
IL-17C and IL-17RE (show IL17RE ELISA Kits) 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 (show IL17RE ELISA Kits) induced the expression of a nuclear IkappaB family member, IkappaBzeta (show NFKBIZ ELISA Kits), in Th17 cells to potentiate the Th17 cell response
Intranasal administration of adenovirus expressing IL-17 (show IL17A ELISA Kits) results in bronchoalveolar lavage neutrophilia and Th1 (show HAND1 ELISA Kits)-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