CTLA4_PIG CTLA4 ELISA tesk kit
- Known as:
- CTLA4_PIG CTLA4 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen15807
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- CTLA4_PIG CTLA4 ELISA tesk kit
Related genes to: CTLA4_PIG CTLA4 ELISA tesk kit
- 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
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- Cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) is a key immune checkpoint in Gastrointestinal system cancers (GSCs), inhibiting T-cell activation by outcompeting CD28 for B7-1/B7-2 binding on antigen-presenting cells, thereby promoting immune evasion. Its overexpression correlates with advanced stage, poor survival, and worse prognosis in gastric, colorectal, esophageal, and pancreatic cancers. CTLA-4 blockade with Ipilimumab or Tremelimumab shows promise, especially combined with PD-1/PD-L1 inhibitors, yielding enhanced antitumor immunity in microsatellite instability-high/deficient mismatch repair (MSI-H/dMMR) tumors with high immune infiltration. However, efficacy is limited by tumor heterogeneity and an immunosuppressive microenvironment enriched in CTLA-4⁺ regulatory T cells (Tregs). Inconsistent clinical responses underscore the need for predictive biomarkers, optimized combinations, and mechanistic insights into resistance. This review explores CTLA-4's role in GSCs, highlighting microenvironment-focused strategies to improve precision and therapeutic outcomes. - Source: PubMed
Publication date: 2026/08/26
Ma FuyuanMa JingyuanLu YaofanXu JingxuanMao JialeYin ZiyueNi ZikunZhao XueqinHuang BiaoQin Yuan - Striae distensae are chronic dermal lesions characterized by extracellular matrix disruption, fragmentation of collagen and elastic fibers, fibroblast dysfunction, and impaired tissue homeostasis. Although platelet-rich plasma (PRP) has regenerative potential, the temporal tissue and immune changes associated with treatment remain incompletely understood. This exploratory longitudinal study investigated histological, histomorphometric, and immunohistochemical changes during subcutaneous autologous PRP treatment in women with post-gestational atrophic abdominal striae. Six participants were allocated to saline-control or PRP groups (n = 3 each) and received weekly applications for 12 consecutive weeks. Biopsies were evaluated at pre-treatment baseline, and after 6 and 12 weeks of treatment using Masson's Trichrome and Weigert's Resorcin-Fuchsin staining, histomorphometry, and immunohistochemistry for IL-6, iNOS, CD163, CX3CR1, CCL5, TGF-β, FOXP3, CTLA-4, and PD-L1. Peripheral-blood platelet counts and platelet concentrations in freshly prepared PRP after separation were assessed throughout treatment. PRP was associated with progressive collagen bundle thickening, improved fiber organization, reduced interfibrillar spaces, and restoration of a denser, thicker, and more interconnected elastic fiber network. These structural changes coincided with time-dependent variations in inflammatory, macrophage-associated, chemokine, regulatory, and immune-checkpoint immunoreactivities. Later samples showed increased CCL5, CX3CR1, iNOS, and TGF-β immunoreactivities, while FOXP3, CTLA-4, PD-L1, CD163, and IL-6 displayed distinct temporal patterns. Collectively, the findings indicate that PRP treatment is associated with coordinated extracellular matrix reconstruction and dynamic immune-stromal remodeling. However, the small sample and single-marker immunohistochemical design preclude causal, functional, or lineage-specific conclusions. These hypothesis-generating observations warrant confirmation in larger studies using standardized PRP characterization, molecular assays, multiplex imaging, and spatial or single-cell approaches. - Source: PubMed
Publication date: 2026/08/25
de Castro Roston José RonaldoRoston Milena Olivieride Arruda Camargo Gabriela Cardosode Oliveira GabrielaReis Ianny BrumLuzo Angela Cristina MalheirosFávaro Wagner José - : Successful translation of cancer immunotherapy is underscored by the efficacy of PD-1/PD-L1 and CTLA-4 inhibitors in the treatment of various malignancies. However, their limited efficacy in glioma indicates alternative immune escape mechanisms. We investigated B and T Lymphocyte Attenuator (BTLA), a co-inhibitory receptor structurally and functionally analogous to PD-1, to determine if it constitutes a key, unaddressed mechanism of immune escape and a novel therapeutic target in glioma. : We analyzed BTLA expression and function within the tumor microenvironment of a Moroccan cohort ( = 44). This was complemented by multiparameter flow cytometry on peripheral blood from glioblastoma (GBM) patients ( = 8) to assess circulating T cell profiles. Findings were corroborated using independent transcriptomic datasets from TCGA and CGGA cohorts. Single-cell RNA-seq and citeSeq identified specific BTLA-expressing cell populations. Elevated BTLA expression was significantly associated with aggressive features and poor overall survival in glioma patients. Mechanistically, BTLA levels were positively correlated with pro-tumorigenic factors, immune infiltration, and immunosuppressive checkpoints. Single-cell and citeSeq analyses revealed that BTLA was primarily expressed by exhausted T cells and conventional type 1 dendritic cells (cDC1) within the GBM microenvironment. Crucially, this phenotype was translated systemically; BTLA defined dysfunctional circulating CD8 and CD4 T cells characterized by diminished IFN-γ production, alongside reduced granzyme B and perforin in CD8 T cells. Our findings indicate that BTLA may represent a relevant pathway associated with an immunosuppressive glioma microenvironment. The therapeutic potential of targeting this pathway, particularly in combination with PD-1/PD-L1 blockade, warrants further investigation. - Source: PubMed
Publication date: 2026/07/25
Souat SanaaEl Azhary KhadijaBourdoukh SaraKone Abdou-SamadQandouci AhmedHarmak ZakiaChoukri KhalilLakhdar AbdelhakimBadou Abdallah - Effective immunotherapy for mismatch repair proficient colorectal cancer (CRC) is lacking. We examined the safety and efficacy of the novel next-generation immune activator/Fc-enhanced CTLA-4 inhibitor botensilimab (BOT) plus PD-1 inhibitor balstilimab (BAL) in the neoadjuvant setting for patients with resectable CRC. - Source: PubMed
Publication date: 2026/08/26
Shah Manish AHissong ErikaJafari Mehraneh DKasi Pashtoon MurtazaAstorkia MaiderKhan SahrishOwens CaseyChen ZhengmingYeo HeatherSocciarelli FabioSarkar SandiptoNguyen AlanaSiolas DespinaOcean AllysonGarrett KellyLowenfeld LeaPigazzi AlessioGuniganti PreethiPatel SanjayBetel DoronHidalgo Manuel - Osteoporosis (OP) is a chronic metabolic bone disease characterized by reduced bone mass, microarchitectural deterioration, and an increased risk of fragility fractures. Although conventional views have emphasized the imbalance between osteoblasts and osteoclasts, advances in osteoimmunology have shown that T-cell subsets regulate bone remodeling through multilayered mechanisms, including the RANKL/RANK/OPG axis, inflammatory cytokine networks, costimulatory molecules, immune checkpoints, the gut microbiota, and cellular metabolic reprogramming. Th17 cells and their signature cytokine IL-17 promote RANKL expression and amplify the NF-κB/MAPK/NFATc1 pathway of osteoclast differentiation, thereby constituting a key pathogenic component in inflammatory bone loss and postmenopausal osteoporosis. In contrast, regulatory T cells (Tregs) inhibit osteoclast formation through Foxp3-, IL-10-, TGF-β-, CTLA-4- and IDO-related pathways, thereby limiting proinflammatory T-cell activation and maintaining bone marrow immune homeostasis. Th1/Th2 cells, CD8+ T cells, γδ T cells, T follicular helper cells, NKT cells, and mucosa-associated unconventional T cells may also influence bone resorption and formation in different pathological contexts through factors such as IFN-γ, TNF-α, IL-4, IL-13, IL-21, IL-22, and membrane-bound RANKL. Drawing on the literature concerning T-cell subsets, the Th17/Tregs and Th1/Th2 balances, γδ T cells, and the RANKL/OPG axis, this review provides a narrative synthesis of current evidence about the molecular mechanisms by which T-cell subsets regulate osteoporosis-related bone remodeling, the features of immune imbalance in different types of osteoporosis, T-cell-targeted intervention strategies, and translational challenges. The aim is to provide a theoretical basis for developing precision antiosteoporotic therapies from an osteoimmune perspective. - Source: PubMed
Publication date: 2026/08/11
Gong YuanZeng WenxingLiao YitaoXie XuanyuQin ZhichaoLi ChaoZhang Xian