Anti-Mouse CD3e FITC 50 ug
- Known as:
- Antibody toMouse CD3e fluorecein 50 ug
- Catalog number:
- 11-0031-81
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD3e FITC 50
Related genes to: Anti-Mouse CD3e FITC 50 ug
- Gene:
- CD3E NIH gene
- Name:
- CD3e molecule
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: Anti-Mouse CD3e FITC 50 ug
Related articles to: Anti-Mouse CD3e FITC 50 ug
- Ampullary adenocarcinoma is rare, and its immune biomarker landscape is incompletely characterized. This article evaluated mismatch repair (MMR), programmed cell death ligand 1 (PD-L1; CD274), and compartment-specific CD3 (CD3E)/CD8 (CD8A) tumor-infiltrating lymphocytes (TIL) in resected tumors and explored associations with disease-specific survival (DSS). Ninety-nine patients underwent pancreaticoduodenectomy at Vancouver General Hospital (VGH) between 1984 and 2013. Duplicate 0.6-mm tissue microarrays (TMA) were assessed for MMR proteins, PD-L1 combined positive score (CPS), and stromal and intraepithelial CD3 and CD8 counts. DSS was estimated using the Kaplan-Meier method. Exploratory Cox models were adjusted for age, histologic subtype, pathologic tumor (pT) group, pathologic node (pN) status, and adjuvant chemotherapy. There were 44 DSS events. MMR deficiency (dMMR) was present in 37 of 99 (37.4%) tumors. PD-L1 was evaluable in 87 tumors; 57 of 87 (65.5%) tumors had CPS ≥1, and 24 of 87 (27.6%) tumors had CPS ≥10. Intraepithelial CD8+ T cells were present in 23 of 98 (23.5%) tumors. PD-L1 CPS ≥1, PD-L1 CPS ≥10, and MMR status were not associated with DSS by log-rank testing (P = 0.35, P = 0.98, and P = 0.74, respectively). In the pT-adjusted model, intraepithelial CD8 presence was associated with lower disease-specific hazard [hazard ratio (HR), 0.422; 95% confidence interval (CI), 0.144-0.994; likelihood-ratio P = 0.048], although the Wald sensitivity test was not significant (P = 0.074). Continuous log-transformed intraepithelial CD8 counts showed a concordant, method-dependent signal. dMMR and PD-L1 expression were common in this historical resected cohort. Intraepithelial CD8 infiltration was associated with DSS, but the borderline and inferential method-dependent estimates require external validation. These prognostic data do not establish benefit from immune checkpoint blockade. - Source: PubMed
Kalloger Steve EChow ChristineGao DongxiaMilne KatyTopham James TKarasinska Joanna MNelson Brad HRenouf Daniel JAird JohnSchaeffer David F - Lymph node (LN) metastasis is a major determinant of prognosis in gastric cancer, yet the immune microenvironment of metastatic versus non-metastatic nodes remains incompletely defined. Spatial resolution of tumor-immune interactions may clarify mechanisms of immune escape associated with nodal progression. We performed compartment-resolved spatial transcriptomic profiling to characterize immune gene expression in gastric cancer LNs. Forty-seven formalin-fixed paraffin-embedded LNs from 13 patients with T2-T4, M0 gastric adenocarcinoma (N1-2: n = 7; N3: n = 6) were analyzed using the NanoString GeoMx Digital Spatial Profiler and an 84-gene immune pathways panel. Twenty-nine non-metastatic and 18 metastatic LNs were profiled. Regions of interest were segmented into tumor and immune compartments, yielding 65 spatially defined compartments. Differential expression was assessed across three comparisons: metastatic versus non-metastatic LNs; metastatic LNs from N1-2 versus N3 patients; and non-metastatic LNs from N1-2 versus N3 patients. Within the immune compartments, non-metastatic LNs showed higher expression of T-cell activation and checkpoint genes (CD3E, CD27, PDCD1, CTLA4), consistent with preserved immune surveillance. Metastatic LNs were enriched for WNT signaling and adhesion-related genes (CTNNB1, ITGAV) and epithelial markers (EPCAM), indicating tumor-driven immune remodeling. N3 metastatic LNs demonstrated increased ICOSLG, IL6, and IFNGR1 expression, suggesting chronic inflammatory activation and immune dysfunction. Notably, non-metastatic LNs from N3 patients upregulated antigen-presentation genes (CD74, HLA-DRB), consistent with early immune conditioning. No significant differences emerged in tumor compartments or pseudo-bulk analyses. Spatial transcriptomic profiling reveals nodal burden-associated immune remodeling, and identifies candidate biomarkers and therapeutic targets for precision immunotherapy in gastric cancer. - Source: PubMed
Publication date: 2026/09/17
Suwatthanarak ThanawatNampoolsuksan ChawisaTanjak PariyadaThanormjit KullanistAcharayothin OnchiraChaiboonchoe AmphunSuwatthanarak TharathornPithukpakorn ManopChalermwai Wipapat VickiSwangsri JirawatMethasate AsadaChinswangwatanakul VitoonParakonthun Thammawat - Spatial immune cell profiling using multiplex immunofluorescence was examined to characterize the inflammatory cell infiltrates and to possibly aid in the distinction of acute cellular rejection (ACR) and lymphocytic bronchiolitis (LB) from its mimickers including bronchus-associated lymphoid tissue (BALT) and infection in lung allograft tissue. Lung allograft biopsies with ACR and/or LB were identified from an institutional pathology lung transplant database (2012-2024). Surgical lung specimens, transbronchial biopsies, and autopsy lungs were used for BALT and infection, respectively. Multiplex immunofluorescence using the PhenoCode Signature Immune Profile Human Protein Panel (CD3e, CD8, CD20, CD68, FoxP3, pankeratin) was performed. The study included tissue specimens with ACR (n = 13), LB (n = 10), BALT (n = 12), and infection (n = 13). The percentage of CD3 + T-cells, CD8 + T-cells, and CD68 + macrophages was higher and the percentage of CD20 + B-cells was lower in ACR, LB, and infection than BALT (p ≤ 0.02, all). The percentage of FoxP3 + CD3 + T-cells was higher in ACR and BALT than infection (p ≤ 0.02, all). In conclusion, ACR and LB are predominantly comprised of T-cells, however B-cells, macrophages, and FoxP3 + CD3 + T-cells are also present. The immune cell composition of ACR and LB is distinct from that of BALT but similar to infection. - Source: PubMed
Publication date: 2026/08/31
Klaisuban WipawiKroneman Trynda NFlotte Thomas JJenkins Sarah MKopp Karla JAubry Marie-ChristineHsu Ying-Han RSaddoughi Sahar AScott John PRoden Anja C - Antigen 85B (Ag85B), an immunodominant protein secreted by (Mtb), induces robust T-cell-mediated immunity in host cells. Previous studies have demonstrated that recombinant BCG strains overexpressing Ag85B (BCG85B) confer significant protection against tuberculosis in mouse models. This study hypothesized that enhanced protection by recombinant BCG85B results from modulation of host immune gene expression by the Ag85B antigen. To test this, RNA-seq analysis was performed on splenocytes from mice immunized with the wild-type BCG (BCG-WT) and BCG85B strains. Differentially expressed genes (DEGs) in the splenocytes of BCG85B-immunized mice indicated upregulation of immune-related KEGG pathways, including Th1/Th2 and Th17 differentiation, NF-kappa B signaling, and cytokine-cytokine receptor interactions, as well as Gene Ontology (GO) processes such as immune response activation, α-β T cell activation, T-cell production and differentiation, IL-15 mediated signaling, and cytokine-mediated signaling pathways and down regulation of metabolic and digestive processes. Additionally, transcription factor (TF) and protein-protein interaction (PPI) analyses confirmed upregulation of genes involved in T cell receptor signaling and immune activation (, , , , , , and ) in splenocytes from BCG85B-immunized mice. Collectively, these findings indicate that Ag85B overexpression enhances adaptive immune activation and reprograms cellular metabolic pathways, thereby increasing vaccine efficacy. - Source: PubMed
Publication date: 2026/08/12
Chauhan VivekKumar RakeshVeerapandian RajaRamos Enrique IJagannath ChinnaswamyGadad Shrikanth SDhandayuthapani Subramanian - BACKGROUNDElucidating immune signals through well-defined cohorts of pediatric acute pancreatitis (AP) and chronic pancreatitis (CP) patients is critical. This study aimed to evaluate plasma chemokine and cytokine levels in pediatric participants with CP, compared with AP and healthy controls (HCs), to identify unique biomarkers of CP.METHODSIndividuals were identified from a prospectively collected pediatric cohort (n = 146). Immunoproteins (n = 247) were measured using the NULISAseq platform on samples from individuals with CP (n = 71), AP (n = 55), and HCs (n = 20).RESULTSThe measured analytes showed separation among the 3 groups (R2 = 0.13, P < 0.001). In the CP group, TRANCE, TWEAK, FLT-1, HGF, and TRAIL were increased when compared with HC and AP patients (FDR-corrected P <0.05). A multivariable logistic regression model including all 5 proteins provided an AUC of 0.94 (0.93-0.96) for differentiating samples from CP versus AP or HC samples. In the AP group, CRP, IL-6, CD3E, ENRAGE, and MIF were elevated compared with HCs, while FGF-2, TAFA-5, IL-33, TRANCE, and CXCL12 were downregulated in the same acute time period (FDR-corrected P < 0.05). In the 21 patients with AP for whom follow-up samples were obtained, there was a notable decrease in sequential expression of IL-6 and CRP over 12 months and increased expression of CCL25, TAFA-5, and TRANCE proteins. Additionally, TRANCE was expressed on CP pancreatic tissue.CONCLUSIONSTRANCE was increased in pediatric patients with CP and decreased in those with AP during a flare. Future studies are needed to investigate the role of TRANCE and other analytes in the pathogenesis of CP. - Source: PubMed
Publication date: 2026/08/24
Farrell Peter RLee BomiAhmed FaizanMoreno-Fernandez Maria EDixit AjayGurria Juan PabloOllberding Nicholas JDuan QingGarlapally VineetChristian PhoebeHusain Sohail ZAbu-El-Haija Maisam