Mouse Anti-Human CD58, FITC-labeled
- Known as:
- Mouse Antibody toHuman CD58, fluorecein-labeled
- Catalog number:
- 128-10047-2
- Product Quantity:
- 1 mg
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Mouse Anti-Human CD58 FITC-labeled
Related genes to: Mouse Anti-Human CD58, FITC-labeled
- Gene:
- CD58 NIH gene
- Name:
- CD58 molecule
- Previous symbol:
- LFA3
- Synonyms:
- -
- Chromosome:
- 1p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-04-06
- Date modifiied:
- 2016-10-05
Related products to: Mouse Anti-Human CD58, FITC-labeled
Related articles to: Mouse Anti-Human CD58, FITC-labeled
- Allogeneic chimeric antigen receptor (CAR) T cell therapies hold promise for certain malignant disorders as they allow for scalability, on-demand availability, and enhanced product quality. Currently, allogeneic CAR T cell approaches focus on deleting the αβTCR complex and MHC-I/II from CAR T cells to prevent GvHD and rejection of allogeneic cells by the recipient's immune system. However, genetic ablation of MHC-I leads to NK activation in recipients due to the "missing-self" response. Here, we demonstrate the successful generation of universal allogeneic CART (UCART) cells that evade the NK cell "missing-self" response and display similar performance to autologous CAR T cells both in vitro and in vivo. An HLA single-chain trimer (ScT) platform enabled our demonstration that HLA-E presentation of a defined signal peptide sequence, VMAPRTLIL (designated as HLA-ESP-1C), confers resistance to NKG2A+ cell populations with negligible activation of NKG2C+ cell populations. Examination of additional receptor-ligand interactions that may impact NK cell activation confirmed that CD54 and CD58 ablation on UCART cells, in combination with HLA-ESP-1C expression, led to optimal resistance to heterogenous NKG2A+/C+ NK cell populations. Finally, in a humanized mouse model reconstituted with allogeneic NK cells, we demonstrate that UCART19 cells promote stringent tumor control. Our work suggests an updated approach for allogeneic CART cell therapy for clinical applications. - Source: PubMed
Publication date: 2026/04/07
Apodaca KimberlyXu ChongStanton Kelsey LBaroja Miren LAlfaro Doblado Angel REngel Nils WWellhauusen NilsCox ArinBerjis AbdullaJi Mei QingBushara OmarMelendez DianaWelch CollinBanerjee EshaAssenmacher Charles-AntoineSheppard Neil CScholler JohnJune Carl HCarreno Beatriz MLinette Gerald P - T cell activation is initiated when T cells recognize their cognate antigen on the surface of antigen presenting cells (APCs). This triggers formation of a specialized membrane interface termed the immunological synapse (IS) which governs the spatial organization of the intercellular protein interactions ultimately determining the T cell response. While this is a fundamental process in adaptive immunity, tools for quantitative analysis and visualization of the IS molecular architecture are lacking. Here we present isMap, a computational framework for automated cell segmentation and quantification of various parameters related to T cell activation and IS formation on supported lipid bilayers (SLBs), including fluorescence intensity measurements, colocalization analysis and radial averaging. We validate isMap by confirming previous results showing that CD58 initially clusters with T cell receptor (TCR) before segregating into a distal ring during synapse maturation in activated CD8 T cells. We also show that PD-L1 is initially distributed across the IS before ultimately accumulating with TCR in the center of the fully mature synapse. ICOSL, CD80 and CD86 cluster in the center of the contact area through all stages of IS maturation and colocalize with TCR in the order of ICOSL>CD86>CD80. These findings demonstrate isMap's utility in dissecting the functional organization of the IS and highlight the dynamic redistribution of ligand-receptor pairs during T cell activation. - Source: PubMed
Publication date: 2026/03/04
Singleton Amanda HolstadManet AnthonyValvo SalvatoreFeenstra MarikeStenmark HaraldDustin Michael LKvalvaag Audun - Primary resistance to chimeric antigen receptor (CAR) T-cell therapies has limited their widespread application. Our prior genome-wide CRISPR/Cas9 screening revealed that the loss of CD58, a crucial intrinsic resistance factor in tumors, resulted in insufficient immune synapse formation and impaired CAR T-cell activation and cytotoxicity. However, the specific signaling pathway and transcriptional changes associated with CAR T-cell dysfunction have not been addressed. Here, we revealed that AP-1-mediated activation was attenuated in CAR T cells impaired by tumor CD58 loss, driving a decrease in mitochondrial biogenesis, metabolic kinetic impairment, mitochondrial membrane potential loss and ROS accumulation. Moreover, this AP-1 attenuation triggered death receptor-independent apoptosis through the intrinsic mitochondrial pathway. In seeking therapeutic strategies, we pharmacologically and genetically blocked three distinct inhibitory phosphatases positioned upstream of AP-1 signaling. Multifaceted validation has demonstrated that dual specificity phosphatase 6 (DUSP6) blockade is an effective approach to supplement AP-1 signaling while notably reducing CAR T-apoptosis and enhancing mitochondrial fitness, proliferation and long-term cytotoxicity. The transcriptomic profiles of DUSP6-ablated CAR T cells revealed markedly upregulated T-cell activation signatures and enriched metabolic pathways. Clinically, bulk and single-cell RNA-seq analyses revealed that DUSP6 was downregulated in patients who responded to T-cell-based immunotherapy, implying its relevance to patient outcomes. Our findings repositioned CD58 not merely as an immune synapse component but also a metabolic checkpoint in CAR T-cell biology, the loss of which triggers AP-1-dependent mitochondrial derangement and creates a permissive landscape for intrinsic apoptosis, which can be ameliorated by ablation of the inhibitory phosphatase DUSP6. Crucially, DUSP6 ablation represents a promising engineering target to potentiate CAR T-cell efficacy in broader applications. - Source: PubMed
Publication date: 2026/03/17
Ma XinranZhang YangWang YaoHan FuxinLu YutingTong ChuanGuo YeleiWei JianshuZhu QiDong LiangCao ZhiMeng ZhenzhenShi JinhongWu ZhiqiangHan Weidong - Primary Biliary Cholangitis (PBC) is a progressive autoimmune liver disorder characterized by immune-mediated bile duct destruction, leading to cirrhosis and liver failure. Current first-line therapy with ursodeoxycholic acid (UDCA) exhibits suboptimal efficacy in 30-40% of patients, underscoring the urgent need for novel therapeutic targets. - Source: PubMed
Publication date: 2026/03/10
Li YinlingXie HuanhuanZhuang ZhenjieFang XinYang WenjunLuo YanHu JiangyiWang WeiWang HaitaoDou XiaobingShi JunpingYang Jin - The multifactorial nature of recurrent pregnancy loss (RPL) requires a comprehensive understanding of its diverse risk factors, including sleep disturbance. Previously, we reported decreased Rev-erbα expression in decidual stromal cells from pregnant mice with sleep disturbance (SD) and patients of RPL with sleep disturbance (RS). - Source: PubMed
Publication date: 2026/02/18
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