CD16b
- Known as:
- CD16b
- Catalog number:
- 1P-214-T100
- Product Quantity:
- 100 tests
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD16b
Related genes to: CD16b
- Gene:
- FCGR3B NIH gene
- Name:
- Fc fragment of IgG receptor IIIb
- Previous symbol:
- FCGR3, FCG3
- Synonyms:
- CD16, CD16b
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-21
- Date modifiied:
- 2019-04-23
Related products to: CD16b
Related articles to: CD16b
- Loss of renal function is associated with premature aging of the immune system; however, earlier studies on this topic enrolled patients with reduced GFR and did not distinguish between those with or without proteinuria. Clinical observations suggest that proteinuria alone might also impair immune defense. It is thus an open question whether patients with a urinary albumin-to-creatinine ratio > 300 mg/g (severe albuminuria) independent of their eGFR have an inflammatory risk profile and a disturbed adaptive immune response. This cross-sectional study included 25 patients with severe albuminuria (uACR > 300 mg/g; P-Group), 19 patients with an eGFR < 60 mL/min 1.73 m2 and a uACR < 300 mg/g (G-Group), and 30 patients with adequate kidney function (C-group). All three cohorts have a similar cardiovascular background with arterial hypertension and coronary artery disease. PBMCs from the patients were challenged with the superantigen Staphylococcal enterotoxin B (SEB) as well as with CMV- and SARS-CoV-2-specific antigens. Monocyte subsets and CD86 and HLA-DR expression were determined through flow cytometry. Transcripts of CD28 and IFN-α and -γ were measured by qPCR. Compared to those in the C-group, patients in the G-group showed a higher polyclonal SEB response and had significantly elevated circulating numbers of inflammatory monocytes (subset CD14++CD16+). CD28 transcripts were decreased in the P-group and G-group compared to the C-group, reaching significance for the G-Group. The CMV- and SARS-CoV-2-specific immune response, as measured by the frequency of CD4+69+137+ T and CD8+69+137+ T cells, was comparable in all three groups. Severe albuminuria per se does not alter the antigen-specific immune response; however, patients with reduced GFR, but not those with proteinuria, show inflammatory and polyclonal immune activation. - Source: PubMed
Publication date: 2026/09/02
Luna Sandoval HumbertoUlrich ChristofMarkau SilkeGirndt Matthias - Severe COVID-19 disease is characterised by a state of hyperinflammation. As key producers of inflammatory mediators in blood, altered inflammatory activity of monocytes within some individuals may contribute to adverse disease outcomes. - Source: PubMed
Publication date: 2026/08/25
Ebrahimnezhaddarzi SalimehAltermatt AimeeKek HansZhou JinglingBoo IreneMcMahon James HGardiner Bradley JSacks-Davis RachelDrummer Heidi EJaworowski AnthonyHearps Anna C - Acute Myeloid Leukemia (AML) is a hematological malignancy characterized by abnormal myeloid cell differentiation, disrupting normal hematopoiesis. This study utilized an integrated computational approach to identify key molecular targets and potential inhibitors for AML therapy. Analysis of the GSE9476 microarray dataset revealed 566 differentially expressed genes (DEGs), including 437 upregulated and 129 downregulated genes. Functional enrichment indicated significant roles in immune response, apoptosis regulation, and hematopoietic pathways. Protein-protein interaction (PPI) network analysis identified ten hub genes-CD44, TNF, IL1B, MYC, STAT1, LCK, CCR7, FCGR3B, MMP9, and CD28-implicated in AML pathogenesis. After examining these ten hub genes' resolution, R-factor, Diffraction Component Precision Index (DPI), least overfitting criteria, and other crystallographic features, we concluded that LCK and MMP9 were the best options for our future research. Pharmit was used to construct and validate an areceptor ligand pharmacophore model based on the crystal structures of LCK (PDB ID: 6PDJ) and MMP9 (PDB ID: 1GKC). Receptor-based pharmacophore models for LCK and MMP9 with AUC values of 0.79 and 0.85, respectively, were constructed and validated by virtual screening. The filtered compounds underwent ADME/toxicity profiling before being precisely docked in the MMP9 and LCK, which was automated using Python scripts, in order to optimize the screening's dependability. Among all screened hits, favorable binding affinity values of -9.7 and -9.9 kcal/mol for CID-56715853 and CID-126445459 with LCK and -8.9 and -9.2 kcal/mol for MCULE-1367186142 and ZINC4896454 with MMP9, respectively, showed significant binding interactions. Molecular dynamics analyses, including RMSD, RMSF, PCA, and MM-GBSA, confirmed complex stability and binding affinity. This comprehensive in-silico framework integrates transcriptomic data, network analysis, pharmacophore modeling, and molecular simulations to identify novel biomarkers and drug candidates for AML, providing a foundation for further experimental validation and therapeutic development. These four hits (CID-56715853, CID-126445459 MCULE-1367186142 and ZINC4896454) are potential candidates for further in vitro and in vivo validation. - Source: PubMed
Publication date: 2026/09/02
Bosu ParthoAdhikary TonmoyRafi Abu SayedIqbal NaveedRasool FatimaAhmed Payer - The cancer-testis antigen MAGE-A4 is an attractive immunotherapy target due to its high expression in various malignancies and restricted expression in normal tissues. Peptides derived from intracellular MAGE-A4 are presented on the cell surface by HLA-A*02:01, enabling targeting by T-cell receptor (TCR)-like molecules. We identified a TCR-like antibody recognizing the HLA-A *02:01-presented MAGE-A4 GVY230-239 peptide complex through yeast-display screening, computational structural prioritization, and experimental validation. Diverging from T-cell engagers, we engineered this binder into a natural killer cell engager (NKCE) by fusing it with a CD16-targeting variable domain of heavy-chain-only antibody (VHH) in an IgG format. This MAGE-A4-directed NKCE demonstrated potent and specific cytotoxicity against MAGE-A4/HLA-A*02:01 tumor cell lines. To distinguish conventional Fc-mediated signaling from VHH-mediated CD16a engagement, we introduced the Fc-silencing N297A mutation. The mutation markedly reduced reporter activation by the parental IgG format, whereas the VHH-containing NKCE retained CD16a reporter activity. Reporter activation was measurable in the absence of target cells and increased further following addition of A375 cells. In cytotoxicity assays, the NKCE mediated target- and CD16a-dependent killing in the tested in vitro models. These findings provide in vitro proof of concept for a MAGE-A4-directed NKCE and support further preclinical evaluation, including cytokine profiling, safety assessment, and in vivo efficacy studies. - Source: PubMed
Publication date: 2026/08/31
Liu YangPeng HongsenFan XingLiu XiaoxiJiao GuandaLi JialinWang TiantianFong Simon JamesZhu LipengDai YenengZhao Qi - Autoimmune neutropenia (AIN) in early childhood is caused by autoantibodies targeting neutrophil surface antigens, most commonly CD16 (FCGR3B), and must be distinguished from congenital neutropenia, malignancy-associated neutropenia and chronic idiopathic neutropenia (CIN). In this study, the diagnostic performance of the cell-based granulocyte agglutination test (GAT) and granulocyte immunofluorescence test (GIFT) was compared with the bead-based LabScreen Multi (LSM) assay in 214-suspected AIN cases. While 36% of samples were positive for anti-CD16 antibodies in GAT or GIFT, only 19% reacted against the same antigen in LSM, primarily against weak or Immunoglobulin M (IgM)-restricted antibody responses. Patients testing positive in all three assays exhibited significantly higher pro-LL-37 levels and lower absolute neutrophil counts (ANCs), indicating preserved granulopoiesis with peripheral destruction. Our findings question the use of LSM as a standalone test in AIN diagnostics. Incorporating pro-LL-37 and ANC in AIN diagnosis may improve differentiation between antibody-mediated neutropenia and other neutropenia forms in children. - Source: PubMed
Publication date: 2026/08/26
Ratcliffe PaulLöfstedt Alexandra HaaraSundin MikaelHöglund Petter