CTLA-4 (CD152), Hamster Anti-Mouse
- Known as:
- CTLA-4 (CD152), Hamster Antibody toMouse
- Catalog number:
- OETAbs116
- Product Quantity:
- 500
- Category:
- -
- Supplier:
- OET
- Gene target:
- CTLA-4 (CD152) Hamster Anti-Mouse
Related genes to: CTLA-4 (CD152), Hamster Anti-Mouse
- Gene:
- CTLA4 NIH gene
- Name:
- cytotoxic T-lymphocyte associated protein 4
- Previous symbol:
- CELIAC3, IDDM12
- Synonyms:
- CD152, CD, GSE, CTLA-4
- Chromosome:
- 2q33.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-25
- Date modifiied:
- 2019-04-23
Related products to: CTLA-4 (CD152), Hamster Anti-Mouse
Related articles to: CTLA-4 (CD152), Hamster Anti-Mouse
- SMARCA4-deficient non-small cell lung cancer (SD-NSCLC) is associated with poor prognosis and lacks a standard treatment strategy. This multicenter retrospective study evaluated immunotherapy-based regimens and characterized the immune features of advanced SD-NSCLC using next-generation sequencing, flow cytometry, multiplex immunofluorescence, single-cell RNA and TCR sequencing, and a CRISPR/Cas9-mediated SMARCA4 knockout model. A total of 162 patients with advanced SD-NSCLC were enrolled from four Chinese cancer centers. Genomic analysis identified TP53, KEAP1, STK11, and KRAS as the primary co-mutated genes. Compared to single-agent chemotherapy, immunotherapy combined with chemotherapy and antiangiogenesis therapy demonstrated significantly longer median progression-free survival (mPFS) (12.10 vs. 2.77 months, p < 0.001). Furthermore, responders to this combination also exhibited elevated CD8 T cell infiltration (p < 0.01). In vivo, the three-drug combination regimen significantly inhibited the growth of SMARCA4-knock-out mouse tumor cells in mice, increased infiltration of CD8 T cells, and reduced the presence of regulatory T cells (Tregs) in the tumor microenvironment. In this mouse model, single-cell RNA-seq revealed a significant decrease in CTLA4 Tregs with active intercellular communication following anti-PD-1 therapy. Ex vivo experiments demonstrated that treatment with anti-PD-1 markedly reduced the proportion of Tregs and concurrently increased the proportions of IFN-γ and TNF-α producing cells. Lastly, single-cell TCR-seq confirmed the expansion of specific TCR clones, particularly within CCR7 and LEF1 naive T cells. Collectively, these findings suggest that immunotherapy-based combination regimens may provide substantial clinical benefit for patients with SD-NSCLC by enhancing CD8 T cell activity, suppressing CTLA4 Tregs, and expanding tumor-reactive TCR clones. - Source: PubMed
Publication date: 2026/07/03
Wu SixuanLi SenyuanZheng YaqinZhang LinlingPan JunfanZhao YunanLin YujunLin JincanPan QihongLin JinhuiChen ShengjiaHuang ZhangzhouLin DongHe MuqunChen YujieHe HaoWang PeiyuanChen SihuiLian RongLi ChaoZhang JingXu HaipengXu Yiquan - High-grade central nervous system cancers incur a significant burden of care on society. The combination of therapeutic resistance and high mortality makes it both a challenging target and a devastating diagnosis. Of these, one in two is characterized as glioblastoma (GBM) with a median survival rate of only 13.5 months with the current standard of therapy. Modern interventions, such as PD-1 and CTLA-4 checkpoint inhibition and autologous CAR T cell delivery, remain stymied by both the difficult nature of drug delivery to the brain and the inherent immunosuppressive tumor microenvironment. However, recent advances in the characterization of GBM have unveiled promising new therapeutic avenues aiming to target and eliminate the tumor. In this review, we summarize the mechanisms through which GBM is initiated, localized, and eludes therapy responses and provide an update on recent advances made within this therapeutic space to overcome GBM-mediated immunosuppression. We also discuss the challenges with current and next generational treatment strategies before finally exploring the landscape of potential future therapeutic targets. - Source: PubMed
Publication date: 2026/07/03
Achari EmersonAhmady-Nield FarahSharma AmitSchmidt-Wolf Ingo G HMaciaczyk JarekLuwor Rodney BAchuthan Adrian A - Acute appendicitis is one of the leading causes of surgical emergency hospitalizations. However, the mechanisms leading to the development of appendicitis are poorly understood. Current knowledge suggests an interplay probably led by dietary habits with impact on the microbiome which elicits responses in genetically predisposed individuals. The aim of this review is to assess the nutrition-microbiome-genetic axis associated with acute appendicitis development. The main dietary and nutritional patterns associated to acute appendicitis were low consumption of fiber, water and fish oil, and high levels of saturated fat, salt, processed meat and ultra-processed foods. Collectively, these westernised dietary patterns (WDP) may increase more than 40% the risk of developing acute appendicitis. The WDP are associated to shifts in the microbiome observed in inflamed appendices such as an increased abundance of Fusobacteria together with a lower level of Proteobacteria. While dietary patterns and associated changes in the microbiome may affect a large proportion of the population, only a relatively small percentage develop acute appendicitis suggesting the existence of predisposing genetic factors. Several single nucleotide polymorphisms (SNP) have been identified linking nutrition and microbiome to the genetic background in acute appendicitis. These include the HLA-C SNP rs2524046, associated with coeliac disease, and the variant rs9953918 of NEDD4L (involved in fluid/water mobilisation). A hypothetical allergy model for appendicitis has been recently proposed providing a preliminary groundwork that identifies SNPs in or near and and involved in the pathogenesis of both inflammatory diseases. - Source: PubMed
Publication date: 2026/07/03
Ryoo MichaelHwang Liang-DarRoura Eugeni - Regulatory CD8 T-cells (CD8 Treg) are a distinct yet understudied T-cell subset capable of simultaneous immunosuppression and cytolysis. Here, we characterized induced human CD8 Treg (CD8-iTreg) generated from peripheral blood CD8 CD25⁻ T-cells using anti-CD3e mAb-loaded artificial antigen presenting cells, IL-2, TGFβ, and Rapamycin. These CD8-iTreg differentiated into a stable, highly proliferative bifunctional population with suppressive activity comparable to CD4-iTreg while retaining cytolytic capacity similar to conventional CD8⁺ cytotoxic T lymphocytes (CTL). Multi-parameter spectral flow cytometry and single-cell RNA-seq revealed a distinct immunoregulatory signature: a predominantly Treg-like profile marked by tissue-residency marker CD103 with increased canonical Treg markers (FoxP3, HELIOS, CD25, CD39, CTLA-4, CCR4, and IL-10) and reduced pro-inflammatory cytokines. A unique cytotoxic program was marked by elevated Granzyme-K (GzmK) and Thrombospondin-4 (Tsp-4), a thrombospondin family extracellular matrix glycoprotein upregulated in activated CD8+ T-cells. Cytolysis was primarily mediated by Perforin (Prf) and multiple Granzymes packaged into Tsp-4⁺ supramolecular attack particles (SMAPs), with GzmK contributing to both cytotoxic and suppressive functions. After anti-CD19scFv CAR (CAR19) transduction, CAR19 CD8-iTreg showed superior anti-tumor efficacy compared with CAR19-CTLs, significantly reducing tumor burden and prolonging survival in a CD19 Nalm-6 human leukemia xenograft model while maintaining low pro-inflammatory cytokine production. In a xenogeneic graft-versus-host disease (GVHD) model with residual human leukemia, CAR19⁺ CD8-iTreg inhibited GVHD lethality and controlled tumor growth without increasing systemic inflammation. Together, these findings support CD8-iTreg-based CAR therapies as a strategy to retain potent anti-leukemic activity while limiting inflammatory toxicities of conventional CAR T-cells, properties particularly beneficial in treating auto- and allo-immune diseases. - Source: PubMed
Publication date: 2026/06/23
Larson Jemma HCompeer Ewoud BDougherty Phillip RSmith KyleZaiken Michael CMargaritaki OlgaKopp BenjaminJin SujeongHarkiolaki MariaChen LinaValvo SalvatoreStaton ClaireCapitani NagajaCassioli ChiaraPayne NathanielBolivar Wagers SaraHani SophiaHoule BaileyPeng YiyunBaldari Cosima TKean Leslie SCantor HarveyDranoff GlennMcDonald-Hyman CameronHippen Keli HDustin Michael LBlazar Bruce R - CAR-T therapy is effective in hematologic cancers but faces challenges in solid tumors due to antigen heterogeneity and an immunosuppressive tumor microenvironment (TME). Systemic CTLA-4 blockade enhances immunity but often causes severe adverse events. To overcome these limitations, we developed a dual-modular nanobody-based CAR-T platform targeting fibroblast activation protein (FAP) on cancer-associated fibroblasts and locally releasing an anti-CTLA-4 nanobody within the tumor stroma. - Source: PubMed
Publication date: 2026/07/02
Li YangziWang XuanZhang ShangkunPeng TaoGong ZihanJiang HaodongHuang XianingXie ShenxiaLiu HengMo FengzhenZhang TongcunYang XiaomeiJiang XiaobingLu Xiaoling