CD72
- Known as:
- CD72
- Catalog number:
- 6L72
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- Hytest
- Gene target:
- CD72
Related genes to: CD72
- Gene:
- CD72 NIH gene
- Name:
- CD72 molecule
- Previous symbol:
- -
- Synonyms:
- LYB2, CD72b
- Chromosome:
- 9p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-10-04
- Date modifiied:
- 2016-10-05
Related products to: CD72
anti-CD72 (4D10)Anti-CD72 AntibodyAnti-CD72 AntibodyAnti-CD72 antibodyAnti-CD72 antibodyAnti-CD72 Polyclonal Antibody (OAAI00031)anti-CD72(4D10)Anti-Mouse CD72.1, Biotin (Clone CT-72.1) (mouse IgG2a)Anti-Mouse CD72.1, FITC (Clone CT-72.1) (mouse IgG2a)Anti-Mouse CD72.1, PE (Clone CT-72.1) (mouse IgG2a)Anti-Mouse CD72.1, Purified (Clone CT-72.1) (mouse IgG2a)Antibodies: CD72, pan B-cell, clone BL-A_A11 Clone: BL-A_A11Antibodies: Mouse Monoclonal to CD72, Species Reactivity: Human, Clone: 3F3, Isotype: IgG2bAntibodies: Mouse Monoclonal to CD72, Species Reactivity: Human, Clone: 3F3, Isotype: IgG2bAntibodies: Mouse Monoclonal to CD72, Species Reactivity: Human, Clone: 3F3, Isotype: IgG2b Related articles to: CD72
- Atherosclerotic cardiovascular disease (ASCVD) remains the leading global cause of mortality, with substantial residual inflammatory risk persisting despite statin therapy. We identify a c-Rel-driven CD72 macrophage subset markedly enriched in human and murine atherosclerotic plaques, whose abundance correlates with disease severity. Single-cell transcriptomics and functional assays demonstrate that CD72 macrophages drive endothelial pyroptosis, oxidative stress and dysfunction via pathological crosstalk through the CXCL12-CXCR4 axis. Through transcriptome-based phenotypic screening, we discover Ilexoside K (IK), a natural triterpenoid saponin, as a dual anti-atherosclerotic and anti-pyroptotic lead compound. Molecular docking, dynamics simulations, and surface plasmon resonance (SPR) validate that IK directly binds CXCR4. In vivo, IK significantly alleviates atherosclerotic plaque burden, dyslipidemia, systemic inflammation and endothelial pyroptosis in high-fat diet-fed ApoE mice with favorable safety. Gain-of-function assays confirm that endothelial CXCR4 overexpression abrogates IK's vasculoprotective effects. This study defines CD72 macrophages as a key pro-atherogenic subset and establishes IK as a promising CXCR4-associated agent for ASCVD treatment. - Source: PubMed
Publication date: 2026/09/27
He XinglingLi SijingChen JiahuiLin LiyuLi XinyuZhang XiaojiaoZhang YihuiChen XinglingGuo JinjianYang ZhongqiLu LuNi Shihao - High-risk MYCN-amplified neuroblastoma is associated with a dire prognosis and often metastasizes to the bone marrow. However, systemic immune remodeling and its effect on the bone marrow niche remain unclear. - Source: PubMed
Publication date: 2026/09/15
Embaie Bethel TesfaiAlchahin Adele MVelentza LillyOlsen Thale KristinGavriliuc Ioana MariaMei ShenglinBaryawno Ninib - This study aimed to evaluate the feasibility of CD72 as a complementary CD19-independent B-lineage gating marker for longitudinal measurable residual disease (MRD) surveillance in relapsed/refractory B-cell acute lymphoblastic leukemia (R/R B-ALL) following CD19 CAR-T therapy. Correlation analyses were performed in 66 B-ALL samples to compare MRD detection using CD72, CD19, and cytoplasmic CD79a. CD72 expression specificity was further evaluated in 129 leukemia patients. In addition, 129 patients with R/R B-ALL treated with autologous CD19 CAR-T therapy in registered clinical trials (ChiCTR-IIh-16008711; NCT03173417) between January 2021 and December 2022 were retrospectively analyzed, with follow-up continued until January 2025. CD72 gating showed excellent concordance with both CD19- and cCD79a-based strategies for MRD assessment. CD72 expression demonstrated high specificity in B-ALL, with a positivity rate of 95.77%, compared with 29.27% in AML and 23.53% in T-ALL. All 129 heavily pretreated patients achieved MRD-negative CR at day 28 after CAR-T infusion and subsequently underwent allo-HSCT, with a median interval of 54 days (range, 40-338). A total of 16 patients experienced MRD relapse during follow-up, including four clinically confirmed CD19-negative relapses that retained CD72 expression. Patients with pre-CAR-T MRD ≤1% showed earlier B-cell recovery than those with MRD >1% (median 30 [18-45] vs. 32 [26-79] days, p = 0.028). The MRD ≤1% cohort demonstrated significantly improved 3-year overall survival compared with the MRD >1% cohort (88.1% vs. 69.2%, p = 0.014). The 3-year cumulative incidence of MRD relapse was significantly lower in the MRD ≤1% cohort than in the MRD >1% cohort (3.96% vs. 17.95%, p = 0.019), while non-relapse mortality was also numerically lower in the MRD ≤1% cohort (5.92% vs. 17.95%, p = 0.053). Multivariate analysis identified KMT2A rearrangement, IKZF1 mutation, TP53 mutation, and elevated pre-CAR-T MRD as independent predictors of inferior outcomes. CD72 represents a feasible complementary B-lineage marker for longitudinal MRD surveillance following CD19 CAR-T therapy. Retention of CD72 expression in clinically confirmed CD19-negative relapses supports its potential utility when CD19 expression is lost after targeted therapy. - Source: PubMed
Publication date: 2026/08/03
Chen ManZhou JingZhao WeiLong JingFu MinjingZhang XianLi YiZhang GailingWang Hui - NC/Jic mice infected with the rodent malaria parasite Plasmodium chabaudi AS (P. chabaudi AS) develop membranoproliferative glomerulonephritis (MPGN), a Type III hypersensitivity reaction. MRL/MpJ-lpr/lpr (MRL/lpr) mice, a murine model of systemic lupus erythematosus, also develop nephropathy, which is classified as a Type III hypersensitivity reaction. This nephropathy in MRL/lpr mice involves cluster of differentiation 72 (CD72), a negative regulator of B cell activation. NC/Jic mice harbored the same Cd72 haplotype as MRL/lpr mice. This haplotype is characterized by a seven amino acid deletion and 13 amino acid substitutions in the C-type lectin-like domain (CTLD) encoded by exon 8. In the present study, we investigated the contribution of the Cd72 haplotype to the development of MPGN in NC/Jic mice. NC/Jic-Cd72 knock-in (NC-Cd72 KI) mice, in which exon 8 of NC/Jic mice was replaced with normal exon 8 derived from the Cd72 haplotype, developed MPGN to a degree comparable to that in NC/Jic mice. In contrast, NC/Jic mice lacking exon 8 of Cd72 (NC-Cd72 Δex8) exhibited significantly attenuated MPGN severity. These results suggest that exon 8 of Cd72 is involved in the development of malaria-induced MPGN in NC/Jic mice, whereas the Cd72 haplotype is not the primary cause. - Source: PubMed
Publication date: 2026/07/30
Miyasaka YukiFujii ShunsukeShibata YukoMasuda YutaKikkawa YoshiakiMizuno MasashiOhno Tamio - PD-1/PD-L1 inhibitor-based chemoimmunotherapy has become a standard first-line treatment for HER2-negative advanced gastric or gastro-esophageal junction cancer. However, most patients eventually experience disease progression, and optimal post-progression strategies, particularly immune checkpoint inhibitor (ICI)-based retreatment, remain unclear. This study evaluated the real-world feasibility of ICI-based retreatment and developed an exploratory tumor microenvironment (TME)-oriented biomarker framework to stratify patients who may benefit from immunotherapy. - Source: PubMed
Publication date: 2026/07/01
Song XueminWu YitingZhu YingmingHe YueqiShi JinjunRen KeGao Chanchan