Mouse Anti-Human CD58, Biotinylated
- Known as:
- Mouse Antibody toHuman CD58, Biotinylated
- Catalog number:
- 128-10046-2
- Product Quantity:
- 1 mg
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Mouse Anti-Human CD58 Biotinylated
Related genes to: Mouse Anti-Human CD58, Biotinylated
- 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, Biotinylated
Related articles to: Mouse Anti-Human CD58, Biotinylated
- The essential role of B cells and B cell intrinsic molecules in tumor immunity is beginning to be recognized. Tumor cell CKLF-like MARVEL transmembrane domain-containing protein 6 (CMTM6) is a novel tumor immunoregulator involved in maintaining membrane levels of several important molecules, such as programmed cell death ligand 1 (PD-L1) and CD58. Host CMTM6 may also play a function in the tumor microenvironment. Here, we found that CMTM6 was highly expressed in splenic B cells and tumor-infiltrating B cells. CMTM6 deficiency resulted in impaired splenic development, germinal center B cell differentiation, memory B cell differentiation, T/B cell interaction and B cell anti-tumor immune responses. Through multi-omics data mining and B-cell agonist screening, we identified that CMTM6 interacted with CD40 and maintained CD40 membrane levels in B cells. CMTM6 -interacts with CD40 and inhibits ubiquitin/proteasome-mediated CD40 degradation. CMTM6 deficiency led to impaired CD40 signaling-mediated B cell activation, survival, proliferation, differentiation and T/B cell interaction. , CMTM6 deficiency leads to a significant decrease in the anti-tumor activity of immune checkpoint blockade (ICB) therapy and B cell-dependent CD40 agonists. Collectively, B-cell intrinsic CMTM6 maintains B cell CD40 levels and signaling to promote B cell function and anti-tumor immunity. - Source: PubMed
Publication date: 2026/07/15
Chen RunqiuChang WenlongLi FanglinGu LonghuaChen ChenZhang RongLi ZhiyingSun JianhuaChen JingGong LikunLong Yiru - Viruses encode immunoevasins that subvert host co-signaling pathways. CD244:CD48 and CD2:CD58 interactions are critical for NK- and T-cell effector responses. We previously identified a herpesvirus-encoded soluble CD48 homolog that functions as a decoy ligand for CD244 and dampens NK-cell activation. Here, we show that this viral protein, A43, also recognizes CD2, and we used its structural features to engineer human CD48-Fc variants with dual CD244/CD2 specificity. The optimized mutein, C5-Fc, which incorporates twelve A43-guided substitutions predicted by structure-based modeling to enhance interface packing and electrostatic complementarity, resulted in high-avidity binding and competitively displacement of native ligands. Fc-silenced C5-Fc (C5-Fc) disrupted NK- and T-cell conjugate formation and reduced CD244- and CD2-dependent cytotoxicity. It also interfered with the maturation of the antigen-dependent immunological synapse and inhibited T-cell proliferation and the secretion of pro-inflammatory cytokines. These data establish C5-Fc as a rationally engineered dual-specificity inhibitor with translational potential for autoimmune diseases. - Source: PubMed
Publication date: 2026/09/01
Bautista-Cerecero OlgaHernández-Luis PabloMartínez-Vicente PabloPoblador FrancescFernandez-Fuentes NarcisOliva BaldomeroMerino-Aboitiz JulenEngel PabloAngulo Ana - Bulky disease represents a clinically aggressive subset of diffuse large B-cell lymphoma (DLBCL) associated with adverse clinical outcomes. The aim of this study was to investigate the influence of oncogenic mutations and tumor microenvironment alterations on bulky disease in DLBCL. - Source: PubMed
Wang Yu-QingWang YueDu Zhi-ShanHuang Xin-YunDong YanTian ShuangFu DiCheng ShuWang LiXu Peng-PengFan Sheng-JinWang Shu-Ye - In this study, we describe the design of peptide aptamers to modulate interactions between CD2 and CD58 (co-stimulatory molecules) in the immune response. We designed peptide aptamers based on the sunflower trypsin inhibitor-1 (SFTI-1) template, incorporating functional groups that confer conformational stability and aqueous solubility. To address the challenges posed by conformational isomerism in the sunflower trypsin inhibitor template due to proline-proline sequences in peptide design, we developed two aptamer peptides, SFTI-FGUA and SFTI-DMY, incorporating specific functional groups. SFTI-FGUA features a side-chain guanidine group on phenylalanine, while SFTI-DMY features a dimethyl group at the meta position relative to tyrosine's hydroxyl group. These bulky substitutions on the phenyl ring effectively restrict conformational flexibility and enhance solubility. Evaluation of these peptides using cell adhesion inhibition assays revealed that both aptamer peptides not only exhibited significant inhibition of cell adhesion but also exhibited a predominant conformation in solution. Furthermore, these peptides exhibited stability against enzymatic degradation. - Source: PubMed
Publication date: 2026/09/02
Chowdhury ArpanShrestha PrajeshSubramanian VivekanandanMayandi VenkateshMahajan MukeshJois Seetharama D - Primary Sjögren's syndrome (pSS) is a chronic autoimmune disorder. Dysregulated interferon-gamma (IFN-γ) signalling is implicated in pSS pathogenesis, yet the underlying mechanisms remain elusive. This study aimed to identify key IFN-γ-associated diagnostic genes and delineate their roles in immune dysregulation using peripheral blood transcriptomic and single-cell RNA sequencing (scRNA-seq) data. Publicly available Gene Expression Omnibus (GEO) datasets were used, and the bioinformatics findings were further supported by reverse transcription-quantitative PCR (RT-qPCR) validation. Peripheral blood transcriptomic data from training and validation cohorts were analysed, and key genes were screened using machine learning algorithms, receiver operating characteristic (ROC) curve analysis, and differential expression analysis. A diagnostic model and nomogram were subsequently constructed. Immune infiltration, pathway enrichment, and gene regulatory networks were also investigated, while scRNA-seq analysis was performed to characterize cellular heterogeneity, pseudotime trajectories, and cell-cell communication. Four key genes, HERC6, IL15, CD58 and PTGS2, were identified, and the resulting diagnostic model and nomogram demonstrated high diagnostic accuracy. Immune profiling revealed marked dysregulation of the immune microenvironment in pSS, accompanied by extensive alterations in metabolic and signalling pathways. Pathway enrichment analysis further demonstrated both distinct and shared functional roles of the four key genes. Single-cell analysis suggested that macrophages may act as central regulators in pSS pathogenesis, as evidenced by altered pseudotime trajectories, enrichment in early differentiation states, and intensified cell-cell communication networks. RT-qPCR further confirmed the significant upregulation of HERC6, IL15, and PTGS2 in patients with pSS. Collectively, this study established an IFN-γ-associated diagnostic model for pSS and implicated macrophages as potential key contributors to immune dysregulation through altered differentiation, enhanced intercellular communication, and IFN-γ-associated gene expression. These findings provide new insights into the pathogenesis of pSS and identify potential diagnostic biomarkers and therapeutic targets. - Source: PubMed
Shi LeiWei Tian-ChiZhang Jing