CD58
- Known as:
- CD58
- Catalog number:
- 10-232-C100
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD58
Related genes to: CD58
- 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: CD58
Related articles to: CD58
- 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 - To evaluate and identify urinary biomarkers for the early diagnosis and staging of diabetic kidney disease (DKD). - Source: PubMed
Publication date: 2026/06/22
Mi MindongXiong TianhuanGong JiyongSun WeijieXu TunguangJiang QifengZhang DanqingZhang JungeHuang JianchengLiang Wei - To characterize the cellular composition and molecular microenvironment of smoking-related periodontitis using single-cell RNA sequencing. - Source: PubMed
Publication date: 2026/06/23
Wang HuiningHu PengxiaoWu JiayuHuang RuiMa JunZhang XiaoxuanYi MengjiaTu JunhaoJia RuiweiZhao ShufanSun XiaoyuHuang Shengbin - Abdominal aortic aneurysm (AAA) represents a high-risk arterial pathology that frequently evolves insidiously and remains without robust molecular tools for timely detection. To identify potential biomarkers with both genetically supported relevance and discriminatory value, we developed an integrated multi-omics framework that synthesizes genetic, transcriptomic, and proteomic evidence. - Source: PubMed
Publication date: 2026/05/29
Xie MingXue YongZhang YufengZhang LeiLi XiandengChen GuobaoLiu JiaHua Haibing - CD3 T cell engagers (TCEs) have transformed hematologic oncology, but dose-liming toxicity and the absence of adequate costimulation have limited TCE success in solid tumors. Consequently, to date, only one classical TCE developed for solid tumors - tarlatamab - has been granted a marketing approval. Here, we report a pioneer combination strategy using a novel CD2-targeted costimulatory bispecific antibody to overcome these limitations. Building on a unique non-blocking CD2 antibody, we developed a HER2×CD2 proof-of-concept bispecific that, combined with an EpCAM×CD3 TCE, provides tumor-dependent costimulation and enhances anti-tumor cytotoxicity mediated by the TCE. We show that HER2×CD2 can be dosed independently to restore optimal anti-tumor cytotoxicity of a sub-efficacious low dose of the EpCAM×CD3 TCE, thus providing a route to avoid TCE-driven toxicity while maintaining efficacy. In a humanized xenograft model, co-treatment with HER2×CD2 achieved complete tumor remission in 8 of 9 mice at a TCE dose that otherwise mediated complete remission in only 1 of 9 mice. We show that HER2×CD2 compensates for the loss of CD58 expression by tumor cells - a well-documented tumor escape mechanism. Notably, unlike CD28-based costimulation, HER2×CD2 effectively also harnessed the anti-tumor cytotoxicity of CD28-negative CD8 T cells - a potent cytotoxic subset prevalent in elderly patients and dominant in solid tumors. Furthermore, HER2×CD2 induced markedly lower cytokine release than a HER2×CD28 bispecific while mediating comparable improvement in anti-tumor cytotoxicity. These findings establish our novel CD2-targeted costimulatory bispecific antibody approach as a promising and potentially safe way to expand and enhance TCE immunotherapy for solid tumors. - Source: PubMed
Publication date: 2026/06/10
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