IL-7 Recombinant Protein
- Known as:
- Interleukin-7 Recombinant Protein
- Catalog number:
- ZR-40-561
- Product Quantity:
- 0.01 mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- IL-7 Recombinant Protein
Ask about this productRelated genes to: IL-7 Recombinant Protein
- Gene:
- IL7 NIH gene
- Name:
- interleukin 7
- Previous symbol:
- -
- Synonyms:
- IL-7
- Chromosome:
- 8q21.13
- Locus Type:
- gene with protein product
- Date approved:
- 1989-10-12
- Date modifiied:
- 2016-10-11
- Gene:
- IL7R NIH gene
- Name:
- interleukin 7 receptor
- Previous symbol:
- -
- Synonyms:
- CD127, IL7RA
- Chromosome:
- 5p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-07
- Date modifiied:
- 2019-04-23
Related products to: IL-7 Recombinant Protein
Related articles to: IL-7 Recombinant Protein
- Adoptive cell therapy (ACT) using TCR-engineered T (TCR-T) cells is a promising strategy for treating solid tumors. One factor that influences the efficacy of ACT is the type of T cells used, with T cells displaying younger, less differentiated or tissue resident phenotypes associated with greater antitumor activity. We aimed to develop a rapid, clinical-scale protocol to generate younger and more potent TCR-T cells for therapy. - Source: PubMed
Publication date: 2026/05/15
Shih Yi-PingDrokin StephanBurke OliviaHuang HuayuLeung AmyBravo-Manriquez MarcoJang MyungkyuSyrkina Marina SJulian LauraSanjuan NelsonTran Eric - Although the clinical burden associated with refractory Mycoplasma pneumoniae pneumonia (RMPP) has been continuously increasing in recent years, the immunological mechanisms of RMPP remain poorly understood. - Source: PubMed
Publication date: 2026/05/29
Yu YanjuanLi ZijieJia GaijingHao ChunboWang GenhaoChen ShouhangWu YangWang FangJin YuefeiTang Yu - Early identification of Alzheimer's disease-related cognitive impairment remains challenging, and existing machine learning (ML) models often suffer from feature instability and limited interpretability. This study developed robust and explainable ML models using cerebrospinal fluid (CSF) biomarkers by systematically comparing sparsity-based (LASSO), importance-based (Boruta), and consensus feature selection strategies. - Source: PubMed
Publication date: 2026/05/29
Cantaş Türkiş Fulden - Crohn's disease (CD) is a chronic inflammatory disorder of the gastrointestinal tract with a relapsing-remitting course. Cytokine dysregulation plays a central role in its pathogenesis, and biological therapies-such as anti‑TNFα agents, vedolizumab, and anti‑IL‑23 monoclonal antibodies-have improved disease control. However, variability in therapeutic response underscores the need for biomarkers to support personalized treatment strategies. A longitudinal study was conducted in 26 patients with clinical‑remission/mild‑activity CD who were treated with adalimumab over 54 weeks. Serum samples were collected at baseline, week 14, and week 54. Eighteen cytokines were quantified using high‑sensitivity Luminex MAP technology. TNFα values were excluded due to drug interference. Clustering and PERMANOVA analyses were used to explore cytokine profiles and their association with disease activity. Four cytokine clusters were identified: Th1‑like, Th2‑like, Th17‑like, and a mixed inflammatory profile including IL‑1β, IL‑2, IL‑12, IL‑21, and IL‑23. Significant reductions in CDAI, C‑reactive protein (CRP), and fibrinogen were observed during treatment. IL‑2, IL‑10, and CCL20 levels increased significantly in patients with active CD (CDAI ≥ 150). Th1 and Th17 signatures were positively correlated with disease activity. Serum assessment of Th1 (IL‑1β, IL‑7) and Th17 (GM‑CSF) signatures generated ROC curves with an AUC of 0.795, compared with CRP (AUC = 0.686) and fibrinogen (AUC = 0.774). Serum cytokine profiling reveals immunological heterogeneity in CD patients treated with adalimumab and may serve as an exploratory biomarker of disease activity and therapeutic response; however, these findings are hypothesis generating and require validation in larger, independent cohorts before clinical applicability can be established. - Source: PubMed
Publication date: 2026/05/29
de Castro-Martínez PatriciaGuijarro Luis GMonserrat JorgeChaparro MaríaGuerra IvánIborra MarisaCabriada José LBujanda LuisAlba CristinaGarcía-Sánchez ValleMarín-Jiménez IgnacioBarreiro-de Acosta ManuelVera IsabelMartín-Arranz María DoloresMesonero FranciscoSempere LauraGomollón FernandoHinojosa JoaquínGómez-Lahoz Ana MGarcía-Montero CieloFraile-Martínez OscarBoaru Diego LÁlvarez-Mon MelchorOrtega Miguel AGisbert Javier P - Atypical peripheral blood cytokine concentrations have been shown in autism, but no clear pattern has been observed. This systematic review and meta-analysis summarised current state of findings, expanded the range of cytokines, accounted for study risk of bias, and examined relations between cytokines and autism traits. Literature comparing peripheral blood cytokine in autistic and non-autistic people was systematically searched in Ovid Embase, MEDLINE and APA PsycINFO, Web of Science and Scopus, resulting in 98 studies and 54 cytokines (4236 autistic, 3333 non-autistic controls; age 2 to 65 years) in the meta-analysis. Study risk of bias was assessed using adapted Newcastle-Ottawa Scale. Compared to controls, autistic people had elevated levels of IL1-beta (Hedges' g = 0.620, 95%CI[0.32, 0.92]), IL4 (g = 0.245, 95%CI [0.07, 0.42]), IL6 (g = 0.365, 95%CI [0.011, 0.62]), IL8 (g = 0.384, 95%CI [0.15, 0.62]), IFN-gamma (g = 0.404, 95%CI [0.09, 0.72]), TNF-alpha (g = 0.31, 95%CI [0.11, 0.51]), CXCL1/GRO-α (g = 0.364, 95%CI [0.058, 0.670]) and MIF (g = 0.560, 95%CI [0.14, 0.98]). Over a third of studies were classified as having a high risk of bias; their removal revealed higher IL7 and IL1RA in autism relative to controls. Narrative synthesis produced no strong evidence for an association between cytokine and autism traits among autistic individuals. Altogether, our findings support a predominance of pro-inflammatory cytokines, while also indicating potential modulatory contributions from inhibitory cytokines, which reflect group-level differences between autistic and non-autistic individuals, but not variations of autism traits within the autistic population. However, higher-quality studies with low risk of bias are needed before firm conclusions can be drawn. - Source: PubMed
Publication date: 2026/05/28
Volk TheresiaLukito SteveRadua JoaquimLuksch HellaRoessner VeitBeyer Nicole