CD72 ELISA kit
- Known as:
- CD72 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CD72-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CD72 ELISA kit
Related genes to: CD72 ELISA kit
- 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
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- 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 - Systemic lupus erythematosus (SLE) is a highly heterogeneous autoimmune disease characterized by persistent immune activation and multi-organ damage. In this study, we integrated network pharmacology, molecular docking, and in vitro validation to identify and prioritize the active compounds, targets, and regulatory pathways of Artemisia argyi (AA). We identified nine candidate active compounds of AA and 380 predicted protein targets. Intersecting these with 218 SLE-associated genes yielded 19 overlapping targets, among which IL2, CASP3, ACE, PPARG, HSP90AA1, and ANXA5 exhibited the highest network connectivity. Functional enrichment analyses highlighted key pathways, including leukocyte activation, IL-17 signaling, and Th17 cell differentiation. Molecular docking revealed favorable binding affinities of quercetin and naringenin with several core targets. Among these, peroxisome proliferator-activated receptor gamma (PPARG) was selected for exploratory validation based on its high network centrality, favorable docking profile, characterized by strong binging affinities (<-5.5 kcal/mol) for both quercetin and naringenin. Subsequent bioinformatic screening identified LTF, CD72, IL13, CHI3L1, and TLR9 as putative SLE-associated genes regulated by PPARG. Experimentally, AA water extract (AAW) upregulated the expression of PPARG and these downstream genes in THP-1-derived macrophages, whereas pharmacological inhibition of PPARG significantly attenuated these effects. These findings suggest that AA modulate PPARG-dependent transcriptional signaling in immune cells, presenting a candidate mechanism that warrants further validation in disease-relevant models. - Source: PubMed
Publication date: 2026/07/10
Luo ManZhou XianleiYan ZimoZhang ZhiZhang Xuemei - Semaphorins are a large family of proteins originally identified for their roles in axon guidance during neural development. Recent findings have established the importance of semaphorins members in modulating diverse immune responses of T cells in vitro and in vivo. Class 3 semaphorins, typified by Sema3A, signal through Neuropilin-1 and Plexin-A receptors in an activation-dependent manner, suppressing effector proliferation while promoting regulatory T cell stability and shaping cytokine profiles in autoimmunity and cancer. Sema3E and Sema3F similarly fine-tune host defense and inflammation by directing Th1/Th17 responses or restraining aberrant chemotaxis. Class 4 members, such as Sema4A and Sema4D, engage Plexin-B1, Plexin-D1, and CD72 to deliver both "forward" co-stimulatory and "reverse" signals: they amplify CD4 and CD8 effector functions, support T helper-B cell crosstalk, and influence tumor immunity via receptor shedding and bidirectional signaling. Finally, although less well defined, class 7 Sema7A operates indirectly-through APCs and Tregs-to regulate inflammatory recall responses and Th1/Th17 driven pathology. Together, these semaphorin-mediated pathways underscore a complex, context-dependent network that balances protective immunity against immunopathology, offering novel therapeutic targets in autoimmunity, infection, and cancer. - Source: PubMed
Publication date: 2026/06/07
Ma HeqingGounni Abdelilah SSu Ruey-ChyiKung Sam K P