Anti-Human CD69 PE 100 tests
- Known as:
- Antibody toHuman CD69 PE 100 tests
- Catalog number:
- 12-0699-42
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Human CD69 100 tests
Related genes to: Anti-Human CD69 PE 100 tests
- Gene:
- CD69 NIH gene
- Name:
- CD69 molecule
- Previous symbol:
- -
- Synonyms:
- CLEC2C
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1992-08-06
- Date modifiied:
- 2016-10-05
Related products to: Anti-Human CD69 PE 100 tests
Related articles to: Anti-Human CD69 PE 100 tests
- The adaptor protein SLP-76 plays a critical role in T-cell receptor signaling and immune activation, yet its relevance in inflammatory bowel disease (IBD) remains unclear. Although calcineurin inhibitors such as cyclosporine A (CsA) are used in severe ulcerative colitis, voclosporin (VCS), a novel calcineurin inhibitor approved for lupus nephritis, has not been systematically evaluated in IBD. We investigated whether SLP-76 is dysregulated in IBD and can be modulated by calcineurin inhibitors. Expression of SLP-76 was analyzed in intestinal biopsy specimens of patients with ulcerative colitis and Crohn's disease using quantitative PCR (qPCR) and immunofluorescence. PBMCs from patients with IBD and healthy control participants were stimulated with anti-CD3/CD28 in the presence or absence of CsA or VCS. Downstream effects were analyzed by qPCR, flow cytometry, cytokine, and metabolic profiling. SLP-76 was significantly upregulated in inflamed intestinal tissue and correlated significantly with histological inflammation. No differences were observed in PBMCs between control participants and patients with IBD. Both calcineurin inhibitors reduced phosphorylation of SLP-76 and impaired downstream signaling in CD4+ and CD8+ T cells. However, only VCS significantly decreased total SLP-76 protein and suppressed expression of the early activation marker CD69 and Ras-MAPL signaling. Metabolomic profiling showed that VCS induced distinct metabolic changes compared with CsA. Our findings highlight SLP-76 as a potential immunoregulatory target in IBD and suggest that VCS exerts broader immunosuppressive effects than CsA, supporting its repurposing as a therapeutic strategy. - Source: PubMed
Loges LauraGabel MichaelKnauss AnnkathrinAtreya RajaGessner ArneBartels NoraNeurath Markus FWeigmann Benno - T-cell engagers redirect cytotoxic lymphocytes toward malignant cells, but their efficacy in solid tumors is limited by uneven antigen expression and inefficient effector-target contact. Here, we report a modular dual-tumor-recognition trispecific T-cell nano-engager (Tri-NanoTCE) generated by Fc-mediated assembly of anti-PD-L1, anti-EGFR, and anti-CD3 IgG1 antibodies on an FcγR1-HSA/PLLA nano-adaptor. PD-L1 and EGFR provide complementary tumor recognition and anchoring, whereas CD3 recruits T cells. Tri-NanoTCE retained the binding activity of all antibodies, showed efficient antibody loading, and increased tumor-cell surface association relative to single-target nano-engagers. This dual-recognition design strengthened effector-target conjugation, enhanced CD69 expression, cytotoxic mediator release, and PBMC-mediated tumor-cell killing, and outperformed free antibody mixtures or dual-component controls. In PBMC-reconstituted MDA-MB-231 and A375 xenografts, Tri-NanoTCE prolonged intratumoral retention, increased human T-cell infiltration, and suppressed tumor growth without obvious short-term systemic toxicity. These findings support modular nanoassembly as a materials strategy for constructing trispecific T-cell engagers for antigen-heterogeneous solid tumors, particularly where target coverage and effector contact are limiting. - Source: PubMed
Publication date: 2026/07/25
Ma Ya-JingZhang ZhengKang Jian-KangChe Xiu-HaiTian Jing-YuanCai Yin-YiShen SongZhao Dong-KunZhu Long - The precise mechanisms underlying the pathogenesis of idiopathic inflammatory myopathy (IIM) remain undefined. However, there has been increasing recognition that tissue-resident memory cells (TRMs) play an important role in the pathogenesis of systemic autoimmune disease. In IIM, TRM-associated transcriptional signatures have been reported, but on a very limited basis. By using multimodal single-cell RNA sequencing analysis in our established murine model of histidyl-tRNA synthetase (HRS)-induced myositis, we identified a prominent population of CD4+ TRMs in inflamed skeletal muscle. Muscle CD4+ TRMs exhibited high expression of genes encoding Cd69, Cxcr6, Runx3, and Prdm1, alongside low expression of Klf2, Ccr7, Sell, S1pr1, and Tcf7 - a profile that is generally consistent with previous reports of TRM gene signature and that we validate through comparison to transcriptomic profiles of human muscle tissue. Detailed pathway analysis in our model indicates that muscle CD4+ TRMs contribute to innate immune regulatory pathways enriched for TNF and IFN-γ signaling. Furthermore, analysis of TCR clonotype distribution and CDR3 sequence similarity revealed pronounced clonal expansion of CD4+ TRMs relative to other T-cell subsets - a pattern that remained stable from 2 to 6 weeks post-immunization. Collectively, these results suggest a potential role for CD4+ TRMs in the pathogenesis of autoimmune myositis. - Source: PubMed
Publication date: 2026/07/23
Li DechengReay Daniel PPinal-Fernandez IagoCasal-Dominguez MariaMammen Andrew LGaffen Sarah LOriss Timothy BAscherman Dana P - The biophysical microenvironment critically shapes T cell activation, yet how nanoscale geometry regulates signaling remains poorly understood. Here, we demonstrate that microvilli insertion into nanopores robustly activates primary human T cells in the absence of TCR ligands, in a pore-size-dependent manner. Nanopores of ∼240 nm in diameter elicit strong ERK phosphorylation, Ca influx, and NFAT nuclear translocation, reaching levels comparable to biochemical stimulation using antibodies against the TCR complex and CD28. Although TCR knockdown attenuates responses, residual CD69 expression upon nanopore engagement indicates that nanoscale confinement lowers the activation threshold. Perturbation of membrane mechanics with GsMTx4 or methyl-β-cyclodextrin, as well as disruption of extracellular Ca-dependent interactions by EDTA, markedly impaired signaling, implicating extracellular calcium and membrane organization as key regulators of signaling. Together, these findings support a model in which ∼240 nm-sized nanopores promote stable close-contact patches that seed TCR signaling. Finally, we show that nanoporous stimulation combined with CD28 costimulation activates patient-derived T cells comparably to conventional methods, highlighting a strategy with translational potential for immunotherapy. - Source: PubMed
Publication date: 2026/07/22
Zünd TamaraLickert SebastianWeber WilliSaxer RafaelWenk MariusZünd JaninaKovalchuk TatianaBaldi LucreziaAghaizu Nozie DDaskalakis MichaelVogel ViolaKlotzsch Enrico - Genetic and preclinical data highlight CD6 as a promising target for multiple sclerosis (MS), yet the impact of clinically available CD6-targeting treatments on MS immunopathogenesis remains insufficiently defined. Itolizumab, a humanized anti-CD6 antibody with established safety and clinical efficacy in other autoimmune disorders, represents a potential candidate to interrogate this pathway in MS. - Source: PubMed
Publication date: 2026/07/21
González-Muñoz CynthiaBaeten PaulienHermans DoryssaHoeks CindyDe Bondt MirreDuran GayelWijmeersch Bart VanSchroten HorstIshikawa HiroshiCrombet-Ramos TaniaLabrada-Mon MayrelBroux BiekeHellings Niels