IL-7, His, Rat Protein
- Known as:
- Interleukin-7, histidine, Rat Protein
- Catalog number:
- z03197-50
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- IL-7 His Rat Protein
Related genes to: IL-7, His, Rat 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
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- BackgroundImmunological dysregulation is a hallmark of Alzheimer's disease (AD), a neurodegenerative disorder characterized by amyloid-β (Aβ) plaque accumulation and hyperphosphorylated Tau protein pathology. AD is associated with altered humoral immunity, which may play a role in its pathogenesis.ObjectiveThis study aimed to investigate alterations in plasma levels of B lymphocyte-associated cytokines and their clinical relevance in AD.MethodsWe performed quantitative detections of 13 cytokines associated with B lymphocytes (TNF-β, IL-13, IFN-γ, TNF-α, IL-2, BAFF, IL-6, CD40L, IL-10, IL-12p70, IL-4, IL-17A, and IL-7) in plasma and analyzed their associations with cognitive functions and biomarkers of AD.ResultsWe found that plasma levels of CD40L, BAFF, TNF-β, IL-6 and IL-17A were increased in AD patients. However, the plasma IL-10 concentrations were decreased in Aβ-PET subjects. Plasma levels of CD40L, BAFF, TNF-β, IL-6, IL-17A were negatively associated with the plasma Aβ ratio. Plasma levels of IL-10 were negatively associated with pTau181. Plasma levels of BAFF were negatively associated with MMSE scores.ConclusionsThese findings demonstrate an altered B lymphocyte-associated cytokine secretion profile in AD patients, which correlates with the clinical severity and biomarkers of the disease. - Source: PubMed
Publication date: 2026/07/07
Wang Meng-TingZhao Rong-ChangHuang MeiChen JiaLi Xin-PengLiu Yu-HuiWang Yan-Jiang - BackgroundConsider this Carrion's disease (CD) is a biphasic illness-comprising acute and chronic phases-endemic to Peru and caused by , a bacterium transmitted by sandflies. Despite its clinical relevance, the mechanisms underlying innate immune activation in response to remain poorly understood. Toll-like receptors (TLRs) play a central role in recognizing conserved molecular patterns present in pathogens, thereby initiating innate immune responses. The present study aimed to describe the expression patterns of TLR2 and TLR4, along with cytokine secretion profiles, during peripheral blood mononuclear cells (PBMCs) exposure to .MethodsPeripheral blood mononuclear cells (PBMCs) from healthy donors were stimulated with heat-inactivated (ATCC 35685 strain), zymosan (TLR2 control), or LPS (TLR4 control). TLR2 and TLR4 gene expression was quantified by RT-qPCR at 0, 12, 24, 36, and 48 h. Cytokines were measured using a 17-plex panel. Analyses were descriptive, using non-parametric statistics.ResultsResults elicited measurable changes in the transcriptional expression of TLR2 and TLR4 during stimulation, with peak activation typically observed at 12 h, although in one case the maximal response was delayed to 24 h. These expression changes coincided with significant modulation of multiple cytokines, including pro-inflammatory mediators (TNF-α, IL-17, IL-12p70), Th1/Th2 cytokines (IFN-γ, IL-2, IL-5, IL-13), regulatory cytokines (IL-10), and growth factors (GM-CSF, IL-7).ConclusionsThis exploratory study describes the transcriptional expression patterns of TLR2 and TLR4 and the accompanying cytokine responses in PBMCs exposed to . These profiles expand current knowledge of the early innate immune signature elicited by this neglected pathogen and provide a foundation for future studies using receptor-specific functional assays. Importantly, these patterns likely reflect early innate immune response signatures rather than definitive evidence of functional receptor activation. - Source: PubMed
Publication date: 2026/07/07
Castillo Angie KEnciso-Benavides JavierMayanga-Herrera AnaRuiz JoaquimGarcía-de-la-Guarda RuthPons Maria J - CAR-T cell therapy has shown remarkable success in hematologic malignancies but remains limited in solid tumors such as liver cancer due to antigen heterogeneity, low target antigen density, and an immunosuppressive tumor microenvironment (TME). Cytokine engineering can enhance CAR-T persistence and effector function; however, the optimal cytokine payload may vary depending on tumor type, target antigen expression level, and microenvironmental context, making systematic experimental comparison time-consuming and labor-intensive. Here, we applied a large language model (LLM)-based CAR-T in silico platform to systematically evaluate cytokine engineering strategies, including IL-2, IL-7, IL-12, IL-15, and IL-18, in glypican-3 (GPC3)-targeted CAR-T cells for liver cancer. We used cytokine selection as a biologically grounded benchmark to test whether the platform could recover known CAR-T cell-relevant cytokine biology and support future novel predictions. Computational predictions identified IL-15 as the most effective enhancer, particularly against tumor cells with low GPC3 expression. Guided by these results, we generated cytokine-armored GPC3 CAR-T cells and performed in vitro and in vivo validation. IL-15-engineered CAR-T cells exhibited superior proliferation, persistence, and serial cytotoxicity against GPC3-low liver cancer cells. In human liver cancer xenograft models, IL-15-enhanced CAR-T cells achieved improved tumor control compared with conventional and other cytokine-engineered CAR-T cells. The recovery of IL-15 served as a positive benchmark supporting the validity of the LLM-guided CAR-T in silico workflow. Collectively, this study establishes an LLM-guided framework, schema-constrained for rational cytokine selection in CAR-T engineering and identifies IL-15 as a potent enhancer for targeting antigen-low liver cancers. - Source: PubMed
Publication date: 2026/07/01
Nan HaochenShen XinyuanYang YouchengWang ShubingLi Yan-Ruide - Invariant natural killer T (iNKT) cells serve as a crucial bridge between innate and adaptive immunity, yet the molecular mechanisms that sustain their subset homeostasis remain incompletely defined. Here, we identify CD23 (FcεRII) as a previously unrecognized intrinsic regulator of NKT17 cell homeostasis. CD23 deficiency selectively diminished NKT17 frequency and IL-17 production in the thymus and spleen, while leaving NKT1 and NKT2 subsets largely unaffected. Loss of CD23 led to decreased IL-7Rα expression and impaired mTORC2-dependent phosphorylation of AKT (Ser473), accompanied by reduced Bcl-2 expression and increased apoptosis of NKT17 cells. Administration of exogenous IL-7 restored NKT17 abundance and IL-17 secretion in CD23-deficient mice without normalizing PLZF or RORγt expression, indicating that CD23 primarily supports metabolic and survival signaling rather than transcriptional programming. Collectively, these findings define CD23 as an upstream checkpoint of the IL-7Rα-mTORC2 axis that preserves NKT17 viability. By delineating a previously unrecognized link between cytokine and metabolic pathways, this study expands the molecular framework governing iNKT cell development and subset maintenance. - Source: PubMed
Publication date: 2026/06/30
Niu LinlinTan BingqianXu JingtingZhang GuangweiWang BoDu ZuochenYang DiZhuang ChengxiDu XiaoyuZhao Yao - Therapeutic modulation of sepsis-induced immune dysfunction by targeting lymphocyte dysfunction with recombinant IL-7 (rIL-7) and anti-PD-1 (e.g. nivolumab) has shown promise in preclinical and early clinical studies. Prior to conducting large randomized controlled trials, an in-depth understanding of the changes induced by rIL-7 or nivolumab (and their differences) in patients with sepsis is imperative. We performed a prospective observational cohort study including patients admitted to the intensive care unit with sepsis and characterized their T lymphocyte phenotype using flow cytometry. The ability of T lymphocytes to respond to a stimulus (using anti-CD3/CD28 beads) and the effect of rIL-7 or nivolumab on T lymphocyte immunophenotype ex vivo was assessed. In a cohort of 55 patients, CD4+ and CD8+ T lymphocyte PD-1 was higher and IL-7R lower compared with healthy volunteers. In a subset of 24 intensive care unit patients in whom in-depth immunophenotype was characterized, ex vivo response of lymphocytes to anti-CD3/CD28 beads was reduced compared with healthy volunteers, simultaneously inducing features consistent with immune activation and immunosuppression. rIL-7 was associated with a greater spectrum of changes compared with nivolumab. The response to rIL-7 and nivolumab was influenced by anti-CD3/CD28 bead costimulation. rIL-7 and nivolumab elicited distinct T lymphocyte responses ex vivo, and the changes were influenced by T lymphocyte activation. It needs to be determined if similar changes occur in vivo, which may influence the choice of immunomodulatory therapy in sepsis. - Source: PubMed
Snow Timothy Arthur ChandosPisciotta WalterMartir GladysCopeland CarolineSekeris AthanasiosDas AbhishekSinger MervynBrealey DavidArulkumaran Nishkantha