MIP_3b
- Known as:
- MIP_3b
- Catalog number:
- ANT-213
- Product Quantity:
- 500µg
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- MIP_3b
Related products to: MIP_3b
Related articles to: MIP_3b
- This study evaluates associations between genetically predicted circulating levels of 91 inflammatory cytokines and juvenile idiopathic arthritis (JIA) susceptibility. Summary statistics for 91 circulating inflammatory cytokines were obtained from a meta-analysis of 11 cohorts comprising 14,824 participants of European ancestry. JIA summary statistics were obtained from FinnGen Release 9 and included 788 cases and 172,834 controls of European ancestry. The primary estimator was the inverse-variance weighted (IVW) random-effects model. MR-Egger, weighted median, simple mode, and weighted mode analyses were used as complementary estimators. Sensitivity analyses included the MR-Egger intercept, Mendelian Randomization Pleiotropy RESidual Sum and Outlier, Cochran's Q, MR-Steiger, and leave-one-out tests. The C-C motif chemokine ligand 19 (CCL19) analysis used 19 independent single-nucleotide polymorphism instruments. At the nominal threshold of P < .05, IVW estimates indicated associations of CCL19 (odds ratio [OR], 2.48), fibroblast growth factor 19 (OR, 0.78), and monocyte chemotactic protein 3 (OR, 0.79) with JIA. After Bonferroni correction for 91 tests (threshold P < 5.49 × 10-4), only CCL19 remained significant (IVW P = 8.93 × 10-8; adjusted P = 8.12 × 10-6). The direction of the CCL19 estimate was consistent across Mendelian randomization methods, although significant heterogeneity and attenuation after outlier correction using Mendelian Randomization Pleiotropy RESidual Sum and Outlier indicated uncertainty in its magnitude. Higher genetically predicted CCL19 levels were associated with greater JIA susceptibility in participants of European ancestry. These findings reflect genetically predicted associations rather than established causal effects and do not support clinical prediction or intervention. Independent genetic, experimental, and clinical validation is required before CCL19 can be considered a biomarker or therapeutic target. - Source: PubMed
Pang JianPan LijiaLiu PingpingQin WanyueYang JinhuaFeng YifeiHe ShengYang Shuihua - Adjuvant anti-programmed cell death protein 1 (anti-PD-1) treatment improves outcomes in high-risk resected melanoma but causes chronic immune-related adverse events (irAEs) in more than 40% of patients. Risk factors associated with chronic vs acute irAEs remain lacking. - Source: PubMed
Publication date: 2026/10/01
Kankaria Roma AFankhauser ReillyBoutros AndreaPinzon MarliesBai KunChen Sheau-ChiannAgbisit Christian BKalyan AlissaLawless AleighaLong Georgina VSullivan Ryan JMehnert Janice MRapisuwon SutheeBalko Justin MCarlino Matteo SMenzies Alexander MJohnson Douglas B - Advanced-stage cutaneous T-cell lymphomas (CTCL) typically manifest as either skin tumor formation or erythroderma; however, exact mechanisms of lesion formation remain insufficiently characterized. - Source: PubMed
Publication date: 2026/09/03
Cohenour Emry RFleischli AbigailMeledathu ShannonNaidu Malini PBuell Caleb AChennareddy SumanthAlkon NataliaJonak ConstanzeJi ZhengKurowski AgataChen ZhihongBrunner Patrick M - Atopic dermatitis (AD) and psoriasis (PsO) are chronic inflammatory skin diseases with distinct features, but clinical and molecular overlap exists. These ambiguous phenotypes complicate diagnosis and treatment, and their immunologic basis remains poorly defined. This study aimed to delineate compartment-specific immune profiles in AD-PsO overlap lesions and explore candidate markers associated with molecular stratification. - Source: PubMed
Publication date: 2026/09/25
Lee JongeunChun Yookyung SophieNam Hyo JeongHuh Yun JungKim JaehwanKrueger James GPaik Seung SamKim Hyun JeJin Seon-PilKim Jeong Eun - Fibrostenotic stricture is a severe complication of Crohn's disease (CD) that affect up to 50% of patients over their lifetime, causing irreversible narrowing of the intestinal lumen and bowel obstruction, but the molecular programs that distinguish stenotic from non-stenotic inflammation and the relative contributions of fibrosis and smooth-muscle remodeling remain incompletely characterized. We aimed to dissect bowel-wall compartment-specific and histology-defined remodeling programs in fibrostenotic CD. - Source: PubMed
Publication date: 2026/09/15
Gui XianyongJin GuangxuCaudell David L