Human Interleukin 17C,IL-17C ELISA Kit
- Known as:
- Human Interleukin 17C,Interleukin-17C Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 201-12-2161
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sunredbio SunBT Sun red bio
- Gene target:
- Human Interleukin 17C IL-17C ELISA Kit
Related genes to: Human Interleukin 17C,IL-17C ELISA Kit
- Gene:
- IL17C NIH gene
- Name:
- interleukin 17C
- Previous symbol:
- -
- Synonyms:
- IL-17C, CX2, IL-21, MGC126884, MGC138401
- Chromosome:
- 16q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-20
- Date modifiied:
- 2016-10-11
Related products to: Human Interleukin 17C,IL-17C ELISA Kit
Related articles to: Human Interleukin 17C,IL-17C ELISA Kit
- Severe trauma triggers a dynamic disturbance of immune function that can progress from early hyperinflammation to prolonged dysregulation, increasing patient vulnerability to infection and chronic critical illness (CCI). To identify immune features linked to different postinjury clinical trajectories, we prospectively evaluated severely injured trauma patients and categorized them as rapid recovery, intermediate, or CCI based on clinical outcome by day 14 of intensive care unit admission. CCI patients developed infections earlier and more frequently than rapid recovery or intermediate patients, with nearly one-third experiencing their first infection (primarily pneumonia) within 4 d of intensive care unit admission and >80% did so within 8 d. Immune profiling showed trauma-associated alterations across all groups, including neutrophilia and early T cell lymphopenia. However, CCI patients exhibited a distinct immunophenotype characterized by elevated neutrophil counts, recovery of total CD3+ T cells by day 7, preserved inducible interferon γ (IFNγ) production, and a selective expansion of CD4+ T helper 17 (Th17) cells. Functional assays revealed sustained or amplified T cell cytokine responses in CCI patients, including persistent IFNγ and interleukin (IL)-17A production. Plasma cytokine analysis further demonstrated prolonged elevation of IL-17A, IL-17C, IFNγ, and IL-10, indicating a mixed but enduring pro- and anti-inflammatory state. These findings suggest that CCI after trauma is not driven by classic immunosuppression, but rather is driven by an IL-17-skewed immune program coupled with ineffective pathogen control. The persistent Th17/neutrophil axis may contribute to heightened infection risk and progression to CCI, highlighting dysregulated IL-17-mediated innate and adaptive circuits as a potential mechanism of ongoing immune dysfunction following severe trauma. - Source: PubMed
Kim Caleb YDing HaiyuanMirabadi NinaLuo ShuhuaScherler KelseyWalters Kathie-AnneO'Keefe GrantGriffith Thomas SBrakenridge Scott C - Idiopathic intracranial hypertension (IIH) is characterised by raised intracranial pressure and disabling headaches, yet its underlying mechanisms remain poorly defined. Calcitonin gene-related peptide (CGRP) is a key neuropeptide implicated in migraine and headache attributed to IIH. CGRP-driven neuroinflammation is implicated in migraine generation but whether CGRP-provoked headache in IIH is accompanied by dynamic neuroimmune activation during the ictal phase remains unknown. We aimed to characterise cytokine alterations during experimentally-induced IIH headache attacks provoked by CGRP. - Source: PubMed
Publication date: 2026/06/13
Yiangou AndreasDo Thien PhuGrech OliviaMugo Caroline WThomas Chloe NGew JessieLange Maria GGee MeganMollan Susan PHill Lisa JLucas Samuel J EAshina MessoudSinclair Alexandra J - This study aims to identify potential biomarkers for retinal detachment secondary to choroidal melanoma (CM). Mendelian randomisation (MR) analysis, immunohistochemistry, cell proliferation and migration assays, co-culture experiments involving human microglial cells (HMC3) and CM cells, and tube formation assay were employed to validate the role of IL-8 in retinal detachment secondary to choroidal melanoma. Mendelian randomisation analysis identified four inflammatory mediators causally linked to malignant melanoma progression: CDCP1 concentration ( = 0.017, OR = 0.999, 95% CI [0.998-1.000]), CSF-1 concentration ( = 0.020, OR = 1.002, 95% CI [1.000-1.003]), IL-10Rβ concentration ( = 0.004, OR = 0.999, 95% CI [0.998-1.000]), IL-17C concentration ( = 0.002, OR = 1.003, 95% CI [1.001-1.005]); Four inflammatory factors exhibited a causal relationship with retinal detachment progression: IL-15Rα concentration ( = 0.029, OR = 1.001, 95% CI [1.000-1.001]), IL-2Rβ concentration ( = 0.007, OR = 1.003, 95% CI [1.001-1.004]), IL-8 concentration ( = 0.045, OR = 1.002, 95% CI [1.000-1.004]), TSLP concentration ( = 0.028, OR = 1.002, 95% CI [1.000-1.004]). MR analysis indicated that genetically predicted IL-8 levels are associated with an increased risk of retinal detachment. IL-8 is highly expressed in CM tissues and promotes the proliferation of CM and HMC3 cells. It partially relieves the inhibitory effects mediated by the supernatant of HMC3 cells and promotes angiogenesis. IL-8 may be involved in CM-related inflammatory microenvironments and secondary exudative retinal detachment. It is a potential biomarker and provides a new target for targeted anti-inflammatory therapy and improved patient prognosis. - Source: PubMed
Publication date: 2026/05/28
Xing ZhenZhang XinranYu WeiLei YingqingWang GuiquLv Hongbin - Immune checkpoint inhibitor (ICI)-based combinations have reshaped systemic therapy for unresectable hepatocellular carcinoma (HCC), yet durable responses remain limited, underscoring the need for mechanism-driven partners that reprogram the cirrhosis-conditioned tumor microenvironment. Here, we synthesize evidence supporting IL-17 family signaling as such a tractable axis and emphasize three translational takeaways. First, "IL-17 blockade" is not a single intervention: canonical IL-17A/F signaling through IL-17RA/RC differs from non-canonical nodes, including IL-17C signaling via IL-17RA/IL-17RE and the dual-ligand IL-17RB node (IL-25 versus IL-17B), which can yield context-dependent-and potentially opposing-effects. Second, HCC-focused models implicate an IL-17A-STAT3-PD-L1 immune-evasion circuit and show that IL-17A neutralization can enhance the activity of PD-1/PD-L1 blockade, positioning IL-17A/F inhibition primarily as an ICI-sensitizing strategy. Third, we argue that clinical translation should prioritize biomarker-guided, etiology-aware early-phase studies with on-treatment pharmacodynamic readouts, rather than unselected monotherapy, while explicitly accounting for infection and gut-barrier risks in cirrhosis. - Source: PubMed
Publication date: 2026/05/28
Pastwińska JoannaKarwaciak IwonaKaraś KajaSałkowska AnnaRatajewski Marcin - Acute postprandial inflammation is a transient response to food intake and may, if repeatedly exaggerated, contribute to chronic low-grade inflammation associated with cardiometabolic disease. A high-fat meal can trigger an acute inflammatory response in the postprandial state, but the role of dietary fat composition remains unclear. The primary aim of the study was to evaluate the effect of different sources of saturated fatty acids (SFA) and Polyunsaturated fatty acids (PUFA) on the postprandial inflammatory response, and the secondary aim was to identify markers of postprandial inflammation. - Source: PubMed
Publication date: 2026/05/12
Limani NamanHenriksen Hege BergMinge Mina MarieSandoval VivianaLandberg RikardLindqvist Helen MHolven Kirsten BUlven Stine MBärebring Linnea