Anti-Mouse CD3e PE 200 ug
- Known as:
- Antibody toMouse CD3e PE 200 ug
- Catalog number:
- 12-0033-83
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD3e 200
Related genes to: Anti-Mouse CD3e PE 200 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 PE 200 ug
Related articles to: Anti-Mouse CD3e PE 200 ug
- Despite marked improvements in survival following preterm birth, the incidence of bronchopulmonary dysplasia (BPD) remains the most prevalent complication of prematurity and carries the risk of long-term morbidity. Characterising the cellular and molecular mechanisms driving disease progression is critical for informing clinical management and improving outcomes. To this end, we conducted a meta-analysis of genome-scale studies to identify molecular pathways implicated in BPD progression in both human cohorts and animal models. - Source: PubMed
Publication date: 2026/07/15
Happs ChrisKhanna PrernaScoynes CharlotteMuriungi NellyAlexander Akira J TRogers Josh ALake ElizabethPickup MaximilianParkinson NicholasMillar Jonathan EBaillie J KennethHendry Sara Clohisey - 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
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