Mouse IL-7 ELISA kit
- Known as:
- Mouse Interleukin-7 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- lf-ek50655
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Abfrontier
- Gene target:
- Mouse IL-7 ELISA kit
Related genes to: Mouse IL-7 ELISA kit
- 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: Mouse IL-7 ELISA kit
Related articles to: Mouse IL-7 ELISA kit
- Chimeric antigen receptor (CAR) T-cell therapies have shown limited promise in solid tumors owing to the immunosuppressive tumor microenvironment. TAK-102 is a next-generation, glypican-3 (GPC3)-targeted CAR T-cell therapy engineered to co-express interleukin-7 (IL-7) and chemokine ligand 19 (CCL19), enhancing T-cell survival and trafficking. In this first-in-human, open-label, phase 1, dose-escalation study (ClinicalTrials.gov: NCT04405778), we evaluated a single TAK-102 infusion in 11 patients with GPC3+ advanced solid tumors refractory or intolerant to standard therapies. Patients received TAK-102 at one of three dose levels following leukapheresis and lymphodepletion chemotherapy. The primary endpoints were the incidences of dose-limiting toxicities, treatment-emergent adverse events, and adverse events of special interest. No dose-limiting toxicities were observed. The most common treatment-emergent adverse events were hematologic, including neutropenia and leukopenia (81.8%), and cytokine release syndrome (54.5%), all grade 1-2. No objective responses were observed; however, five patients achieved stable disease (disease control rate, 45.5%). One patient had a 26.1% reduction in tumor size lasting 9 months, accompanied by a 51.6% decline in serum alpha-fetoprotein. Cellular kinetics showed dose-dependent expansion, with the highest exposure at 5 × 10⁸ CAR+ cells/body. Post-treatment biopsies revealed increased CD8+ T-cell infiltration and activation markers, although CAR+ cells were undetectable in tumor tissue. Serum CCL19 levels increased with dose, suggesting immune priming. These findings support a manageable safety profile for TAK-102 and provide early evidence of biological activity in solid tumors. Further studies are warranted to optimize dosing, improve CAR T-cell persistence, and evaluate efficacy in larger patient cohorts. - Source: PubMed
Publication date: 2026/09/08
Kuboki YasutoshiKoyama TakafumiIkeda MasafumiSatake TomoyukiSawada TakeshiShimazu YutakaKondo ShunsukeKatsuya YukiKagehara HideakiAkaike TakenoriSingh AmanAtkuri KondalaPop-Damkov PetarTamada KojiNakajima Takako Eguchi - AAA ATPase p97 is a central regulator of protein homeostasis, yet its role in late-stage thymocyte development remains undefined. Here, we demonstrate that T-cell-specific ablation of p97 in mice severely blocks the double-positive (DP) to single-positive (SP) transition, with a pronounced defect in CD8 lineage commitment. Using both genetic deletion and acute pharmacological inhibition, we revealed a stage- and lineage-specific requirement for p97, with DP thymocytes being most sensitive to p97 loss. This failure in late-stage positive selection leads to intrathymic developmental arrest of immature DP cells and profound peripheral T-cell lymphopenia. Mechanistically, p97 deficiency results in the accumulation of ubiquitinated proteins, triggering the unfolded protein response and apoptosis in thymocytes. Furthermore, we identified a critical requirement for p97 in sustaining IL-7 receptor (IL-7R) expression and JAK signaling. Strikingly, pharmacological activation of JAK partially rescued SP thymocyte development in p97-deficient mice. Our findings establish p97-mediated protein homeostasis as a previously uncharacterized, cell-intrinsic checkpoint that is indispensable for late-stage positive selection by preventing proteostatic collapse and ensuring the fidelity of IL-7R signaling. - Source: PubMed
Publication date: 2026/09/07
Yu RuixianZhang WeihongHan YiWang WenjiaMeng YanNie PingpingZhang CuiweiYe ZaishengYan BinZhou ZhaocaiJiao Shi - Extrapulmonary tuberculosis (EPTB) represents a substantial proportion of tuberculosis cases, particularly among people living with HIV. Tuberculous lymphadenitis is one of the most common forms of EPTB and represents a condition in which the lymph node functions both as an immune-organizing site and a focus of Mycobacterium tuberculosis (Mtb) infection. Although peripheral blood biomarkers are frequently used to investigate immune responses in tuberculosis, they may not accurately reflect immunological processes occurring at the site of disease. In this study, we aimed to characterize and compare systemic and local inflammatory responses in individuals with suspected lymph node tuberculosis. We conducted a case-control study including 24 individuals undergoing lymph node biopsy for pathological lymphadenopathy at the National Institute of Infectious Diseases Evandro Chagas (Fiocruz), Brazil. Eleven participants were diagnosed with tuberculous lymphadenitis (45.8%) and thirteen served as non-TB controls (54.2%). Paired plasma and lymph node interstitial fluid samples were collected, and concentrations of 29 cytokines, chemokines, and growth factors were quantified using multiplex Luminex assays. Statistical analyses included non-parametric comparisons, hierarchical clustering, Spearman correlation-based network analysis, and canonical correlation analysis to evaluate inflammatory profiles and immune network organization. Plasma inflammatory profiles did not distinguish EPTB cases from controls. In contrast, lymph node samples from EPTB participants exhibited significantly higher concentrations of IL-8, IL-3, and IL-5 and reduced IL-10 levels. Network analyses of correlations between protein concentrations revealed dense and highly interconnected inflammatory networks in plasma, centered on IL-6, IFN-α2, and IL-12p70, whereas lymph node networks were sparser and dominated by TNF-α and IL-1 family cytokines. Cross-compartment analysis identified associations between systemic mediators, particularly TNF-β and IL-7, and pro-inflammatory signals in lymph nodes. Additionally, HbA1c levels were correlated with concentrations of multiple inflammatory mediators, particularly within lymph nodes. Together, these findings indicate that tuberculous lymphadenitis is characterized by marked compartmentalization of immune responses, emphasizing the importance of tissue-level immune profiling for understanding EPTB pathogenesis. - Source: PubMed
Publication date: 2026/09/05
Vinhaes Caian Lda Silveira Samyra AlmeidaBarreto-Duarte BeatrizAndrade Bruno BSant'Anna Flávia MarinhoSchmaltz Carolina Arana StanisRidolfi Felipe MRolla Valeria CGomes-Silva Adriano - Delayed graft function (DGF) is a common early complication of kidney transplantation characterized by immune activation. The duration of DGF may significantly affect long-term graft survival, yet the immune mechanisms underlying the different DGF durations remain unclear. Using a functional definition of delayed graft function (fDGF), defined as a failure of serum creatinine to decrease by at least 10% per day for three consecutive days within the first postoperative week, patients were stratified into short-term DGF (SDGF) and long-term DGF (LDGF) groups according to recovery periods. In this exploratory study, targeted proteomic analysis indicated that proteins enriched in SDGF were primarily involved in innate immune responses and acute inflammatory processes, including neutrophil chemotaxis and migration, whereas LDGF exhibited features related to adaptive immune responses and chronic inflammation, such as T-cell differentiation and activation. IL-7 and CCL20 were identified as candidate molecules potentially associated with different DGF durations. Targeted metabolomics revealed disturbances in amino acid metabolism, particularly alanine, aspartate, and glutamate metabolism, as well as in energy metabolism, including the tricarboxylic acid (TCA) cycle, which may be involved in LDGF. These findings provide preliminary insights into immune metabolic features associated with different DGF recovery durations. - Source: PubMed
Zheng YaxinDai YongZhou FengyingLuo HaiyuWang BaoyaoLai LiushengLiao QiZou YaoshuangHuang LingyuLiu JunhongWang FengyingChen HuaizhouTang DongeYan Qiang - Neuroinflammation and systemic immune dysregulation are increasingly recognized as key contributors to secondary brain injury after aneurysmal subarachnoid hemorrhage (aSAH). However, the temporal relationship between circulating cytokine responses and innate-like lymphocyte populations, particularly mucosal-associated invariant T (MAIT) cells, remains poorly characterized. - Source: PubMed
Publication date: 2026/08/20
Merei AkosBalazs NoemiChayeen Brotzki Da CostaEngelmann PeterBerki TimeaErdő-Bonyár SzabinaSimon DianaMolnar TihamerOlah CsabaCsecsei Peter