CD48
- Known as:
- CD48
- Catalog number:
- 11-226-C100
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD48
Related genes to: CD48
- Gene:
- CD48 NIH gene
- Name:
- CD48 molecule
- Previous symbol:
- BCM1
- Synonyms:
- BLAST, mCD48, hCD48, SLAMF2
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
Related products to: CD48
Related articles to: CD48
- 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 - Paraquat (PQ) is a globally and widely used high-residue herbicide, also regarded as a potential environmental risk factor for neurodegenerative diseases (NDs). However, how PQ exerts neurotoxicity remains a mystery. The blood-brain barrier (BBB) plays a crucial role in communicating between the central nervous system (CNS) and the peripheral blood. In this article, the core genes, which were mainly based on the potential targets for PQ, MPTP, and Diquat chemicals from the CTD database, intersected with the potential targets related to the symptoms of NDs from databases GeneCards and OMIM. Then GO and KEGG enrichments revealed IL-17A was involved. After being treated with PQ, in vivo, C57BL/6J mice showed low mood and decreased learning and memory abilities. Pathologically, there were captured CD3 and its CD4/8 subsets, as well as IL-17A. Surprisingly, T cells in peripheral blood and spleen that responded to PQ gradually leaned towards Th17 cells and secreted IL-17A. Therefore, it is highly suspected that IL-17A plays a role in disrupting the BBB. In vitro, constructed with recombinant IL-17A, and single-PQ or mixtures (recombinant IL-17A and PQ) to bEnd.3 cells, which together showed that IL-17A is a helper for PQ to aggravately disrupt the BBB. In vivo, mice were treated with IL-17A neutralizing antibodies, which effectively inhibited the permeability damage of the BBB. And in the brain parenchyma, the expression of IL-17A also decreased. In summary, the first to respond to PQ were T cells in the peripheral blood, mainly secreting IL-17A, which also acted as a risk factor disrupting the BBB and assists PQ and other factors in infiltrating parenchyma. - Source: PubMed
Publication date: 2026/08/25
Shi GeWang KaidongWang TaoZhang XinyuLiu QinJiao YuxuanQi AiHuang Min - Chimeric antigen receptor (CAR) T cell therapies have revolutionized treatment of hematologic malignancies such as lymphoma and multiple myeloma. However, their success is limited by high manufacturing costs, reliance on autologous T cells, variable product quality, and life-threatening toxicities like cytokine release syndrome. In contrast, natural killer (NK) cells offer a safer, more flexible alternative, but their clinical translation remains constrained by complex expansion protocols and high production costs. Here, we present a transformative approach using the human NK cell line YTS, which is amenable to large-scale culture, genetic manipulation, and cryopreservation. By introducing a CD19-specific CAR into YTS cells, we generate potent effector cells capable of selectively eliminating CD19-expressing targets. We demonstrate that CAR signaling in YTS cells requires intracellular activation and, in certain tumor settings, is enhanced by co-stimulation via the 2B4-CD48 pathway. Importantly, irradiation of YTS-CAR cells prevents proliferation without compromising their cytotoxic function even after freezing and thawing. In preclinical models, injections of irradiated YTS-CAR cells significantly reduced CD19+ tumor burden, underscoring their therapeutic promise. This work positions engineered YTS cells as a novel, scalable, and cost-effective "off-the-shelf" immunotherapy platform suitable for treating refractory leukemias and lymphomas. Future studies will be required to assess safety and to explore applicability to autoimmune diseases and solid tumors. - Source: PubMed
Publication date: 2026/08/13
Jaber HananKhalaf Anas AbuWeiss LolaCohen ItayBannoura NataliOsaili TamaraMaximov OrtalChaouat Abigael EvaKournos MarkTabib AdiMevorach DrorEngel YardenBerger MichaelMandelboim OferElias Shlomo - Cluster of differentiation 48 (CD48) is a glycosylphosphatidylinositol-anchored member of the signaling lymphocyte activation molecule (SLAM) family that is predominantly expressed on hematopoietic cells and regulates immune-cell communication through 2B4 (CD244) and CD2. This narrative review critically summarizes the context-dependent role of CD48 in tumor immunity, with emphasis on the distinction between activating trans-interactions and potentially inhibitory cis-interactions. Evidence from hematologic malignancies and selected solid tumors indicates that CD48 may support antitumor immunity by facilitating natural killer (NK) cells activation, CD8 T-cell co-stimulation, immune synapse formation, and effector cytokine production. Conversely, loss of CD48 expression, sustained CD48-2B4 engagement, altered ligand density, and suppressive myeloid-rich tumor microenvironment (TME) may contribute to immune escape or NK cells dysfunction. Current therapeutic concepts, including anti-CD48 monoclonal antibodies, antibody-drug conjugates, bispecific antibodies, engineered NK/T cells, and epigenetic restoration of CD48 expression, remain largely preclinical and require cautious interpretation. Major translational barriers include broad CD48 expression on normal hematopoietic populations, soluble CD48 (sCD48) interference, uncertain biomarker standardization, and the risk that forced activation in dense solid tumors may reinforce cis-inhibitory signaling rather than improve cytotoxicity. Future studies should define tumor-type-specific signaling states, quantify sCD48, integrate spatial and single-cell approaches, and evaluate rational combinations with programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1) blockade in mechanism-driven models before clinical translation. This review aims to critically evaluate the dual regulatory roles of CD48 in tumor immunity, distinguish between activating trans-interactions and potentially inhibitory cis-interactions across different tumor types, and assess the translational potential and challenges of CD48-targeted immunotherapeutic strategies. - Source: PubMed
Publication date: 2026/07/16
Lin ZhenanChen ZhongwuDeng ZihuaBao TingtingShen Sandi - Periodontitis is a chronic inflammatory disease characterized by progressive destruction of periodontal supporting tissues, yet the molecular mechanisms underlying its pathogenesis remain incompletely defined. This study aimed to identify key genes associated with periodontitis through an integrative bioinformatics strategy combined with experimental validation. - Source: PubMed
Publication date: 2026/07/02
Gu YueBu MingyangSun JingyuanLiu JuanYu LixianYuan XuriXing CongcongHan KaixuanLiu LiangShen XiaoDanYang YakunLiu Qing