IL-17A, Mouse Protein
- Known as:
- Interleukin-17A, Mouse Protein
- Catalog number:
- z03031-1
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- IL-17A Mouse Protein
Related genes to: IL-17A, Mouse Protein
- Gene:
- IL17A NIH gene
- Name:
- interleukin 17A
- Previous symbol:
- CTLA8, IL17
- Synonyms:
- IL-17A, IL-17
- Chromosome:
- 6p12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-10-25
- Date modifiied:
- 2019-04-23
Related products to: IL-17A, Mouse Protein
Related articles to: IL-17A, Mouse Protein
- Psoriasis is a chronic inflammatory skin disease driven by the synergistic interplay between aberrant epidermal proliferation and immune imbalance, with its core pathological process centered on the IL-23/IL-17 inflammatory axis. In recent years, accumulating evidence has demonstrated that calcium (Ca) signaling not only participates in keratinocyte (KC) differentiation and the maintenance of skin barrier homeostasis but also serves as a critical upstream regulator of the maturation and activation of immune cells, including dendritic cells (DCs), Th17 cells, neutrophils, and mast cells. This review systematically summarizes the mechanistic roles of Ca signaling dysregulation in psoriatic keratinocytes and multiple immune effector cells, with particular emphasis on the regulatory functions of SOCE within the DC-Th17 inflammatory axis. Current evidence indicates that the collapse of epidermal structural support systems, impaired Ca sensing, and SOCE dysfunction collectively contribute to insufficient local Ca signaling and defective KC differentiation. In contrast, persistently activated Ca-dependent signaling within the immune compartment promotes Th17 polarization, IL-17A release, and inflammatory cascade amplification through downstream pathways including Calcineurin-NFAT-RORγt. Based on these observations, this review further proposes that "compartment-specific bidirectional calcium dysregulation" may represent an underrecognized pathological pattern in psoriasis, characterized by the coexistence of impaired epidermal calcium signaling and persistent immune calcium hyperactivation. Furthermore, this review discusses therapeutic strategies targeting Ca signaling and their translational challenges, including SOCE-targeted interventions and future combinatorial therapeutic approaches. Overall, this review reappraises the pathogenesis of psoriasis from the perspective of Ca signaling with the aim of providing a novel theoretical basis for future precision immunomodulation and the development of innovative therapeutic strategies. - Source: PubMed
Publication date: 2026/07/15
Chen Y XZhuo D XWang F F - Chronic epididymo-orchitis contributes significantly to male infertility through immune cell infiltration and pro-inflammatory cytokine elevation. High glucose intake promotes Th17 differentiation and autoimmunity, but its effects on autoimmune testicular inflammation remain unclear. - Source: PubMed
Liu Jin-ChuanZeng Qun-XiongShi FuShi JiangxiaLiu XiaofengLyu MinminLi YuJannini Emmanuele ADuan Yong-Gang - The global burden of psoriatic arthritis (PsA) is considerable, with major effects on both quality of life and life expectancy. Approximately 40-50% of patients do not achieve the established therapeutic targets. Challenges related to tolerance, compliance, and therapeutic escape persist. - Source: PubMed
Publication date: 2026/07/29
Osunbor OsariemenNkeck Jan RenéAdebajo Adewale O - Macrophage NLRP3 activation is crucial for antifungal immunity, yet its role in chromoblastomycosis-a chronic subcutaneous mycosis typically caused by -remains unclear. Unlike prior self-resolving models using conidia and hyphae, clinical disease features muriform cells, a parasitic form resistant to macrophages and linked to chronicity. Notably, chitin, a weak NLRP3 agonist, accumulates on the surface of muriform cells. This study investigates whether chitin accumulation modulates NLRP3 activation and promotes fungal persistence. - Source: PubMed
Publication date: 2026/07/14
Chen YaoQu ZiluXie ZhaolanWang XiaowenTong ZhongshengYang LuoyaoZhang XuChen LiuqingDong Bilin - Cardio-renal-metabolic syndrome (CRMS)-characterized by the pathological interplay of visceral adiposity, insulin resistance, chronic kidney disease, and cardiovascular disease-affects over 90% of US adults across its staging spectrum, yet its multi-organ burden remains difficult to assess non-invasively at the point of care. This narrative mini review examines whether multiparametric ultrasound within a single examination can serve as an integrated imaging biomarker set complementary to established molecular markers of CRMS. A narrative search of PubMed (2015-2026) was conducted using PICO-structured queries. The hepatic controlled attenuation parameter and liver stiffness measurement correlate directly with Homeostatic Model Assessment of Insulin Resistance (HOMA-IR), CRP, and adipokine dysregulation, with pooled CAP cutoffs of 268-313 dB/m and elastography thresholds of 8.2-13.6 kPa for fibrosis staging in MASLD. Epicardial adipose tissue thickness correlates with circulating IL-17A (r = 0.308), hs-CRP (r = 0.666), and HOMA-IR (r = 0.567-0.580), independently predicting left ventricular diastolic dysfunction beyond BMI. Carotid intima-media thickness tracks eGFR decline longitudinally and predicts cardiovascular mortality in CKD populations. Renal resistive index, with a validated threshold of ≥0.70, independently predicts GFR decline and cardiovascular mortality across diabetic and hypertensive populations. Renal shear wave elastography distinguishes fibrotic from non-fibrotic parenchyma, with 93.1% sensitivity against biopsy. Cross-compartmental correlations and composite imaging-biochemistry models consistently outperform single-parameter approaches. Two critical gaps remain: specific ultrasound values have not been associated with AHA/ACC CKM stages, and no outcome study has validated a multiorgan protocol. Multiparametric ultrasound provides a clinically feasible, evidence-based CRMS assessment that remains to be validated in prospective trials. - Source: PubMed
Publication date: 2026/07/14
Kutek Marcin LWitkowski Jacek M