Ask about this productRelated genes to: CD166 antibody
- Gene:
- ALCAM NIH gene
- Name:
- activated leukocyte cell adhesion molecule
- Previous symbol:
- -
- Synonyms:
- CD166, MEMD
- Chromosome:
- 3q13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1997-01-17
- Date modifiied:
- 2016-10-05
Related products to: CD166 antibody
Related articles to: CD166 antibody
- Adenoid hypertrophy (AH) is associated with excessive proliferation of germinal center B (GC-B) cells, yet the mechanisms underlying GC regression and termination remain poorly understood. This study used single-cell RNA sequencing (scRNA-seq) to profile the cellular composition of GC-B cells in AH. A unique subset of GC-B cells expressing CD9 was identified through comprehensive scRNA-seq, flow cytometry, and Mass cytometry (CyToF) analyses, with subsequent studies assessing the roles of CD9 and FOXP1 in GC-B cell differentiation and apoptosis pathways. CD9 B cells were detected throughout GC-B cell development and were regulated by FOXP1. These cells also exhibited activation of cell death-related pathways, particularly during adenoid development. AH samples showed an increase in T follicular helper (Tfh) cells, accompanied by a reduction in CD9 B cells. In Cd9 knockout mice, CD9 deficiency led to a significant decrease in serum IgG levels. Further analysis revealed that CD9 B cells promoted Tfh cell apoptosis via pathways such as ALCAM-CD6. CD9 B cells may regulate GC-B cell regression by inducing Tfh cell apoptosis, and FOXP1 may play a role in their differentiation. These findings clarify mechanisms of GC degeneration and termination, offering potential targets for AH treatment. - Source: PubMed
Publication date: 2026/08/30
Liao WenjingSong LijuanXu MeiqianLiang TianhaoChen YixuanChen GuiLin ZaihuanDu HuakangFeng GuofeiFeng ZhimingZhang QiPan FanYang SaixuanZhang XinyinPeng WenxuLi TianlongLin ZhuoshenChen YabangLiu JiayiPeng BaoxinLiu YanNiu XingLi TingHuang ChengyuMo KeXie JianleiZou YuZhang Xiaowen - Intervertebral disc (IVD) degeneration, a leading cause of chronic lower back pain, is associated with loss of vacuolated notochordal cells (NCs) and fibrotic remodeling of the nucleus pulposus. Emerging therapies increasingly focus on NCs, which are rare but therapeutically relevant cells for regenerating degenerated IVDs. In this study, we used CRISPR-based transactivation (CRISPRa) to direct the differentiation of human induced pluripotent stem cells (iPSCs) into the NC lineage. We tested CRISPRa-mediated activation of NOTO, TBXT, FOXA2, SOX5, SOX6, and SOX9, coupled with single-cell sequencing of Aggrecan-2A-mScarlet reporter iPSCs. This approach identified the SOX5/6/9 combination (SOX-trio) as critical for promoting NC lineage commitment. The SOX-trio yielded the largest cell population expressing a range of genes previously associated with NC identity, including SHH, FOXA1, FOXA2, FOXJ1, FN1, ALCAM, KRT8, and KRT18. Our study demonstrates the integration of CRISPRa with single-cell technologies as a powerful platform for investigating and enriching iPSC-derived NCs, supporting future regenerative strategies across various fields. - Source: PubMed
Publication date: 2026/08/27
Tong XiaoleVisscher MariekeRiemers Frank MVersluis DanielleGeijsen NielsShang PengTryfonidou Marianna APoramba-Liyanage Deepani W - Triple-negative breast cancer (TNBC) is associated with recurrence, metastasis, and limited durable responses to immunotherapy, in part due to persistence of breast cancer stem cells (BCSCs). We investigated whether CD6-directed immunotherapy with the monoclonal antibody UMCD6 enhances immune-mediated killing and alters function of BCSC in stem cell-enriched TNBC models. The SUM-149 and SUM-159 cell lines were analyzed for CD6 ligand expression, cocultured with human peripheral blood mononuclear cells (PBMCs) treated with UMCD6, pembrolizumab, or isotype control, and assessed by live-cell cytotoxicity imaging, flow cytometry, soft agar colony formation, and extreme limiting dilution sphere assays. Both TNBC lines co-expressed the CD6 ligands CD44, CD166/ALCAM, and CD318/CDCP1. UMCD6 significantly increased PBMC-mediated apoptosis and reduced tumor cell survival in both models, with greater activity than pembrolizumab under these in vitro conditions. In surviving SUM-159 cells, UMCD6 reduced the ALDH population wit×hout significantly altering CD44CD24 frequency, indicating preferential effects on a distinct stem-like compartment. Functionally, UMCD6 decreased anchorage-independent colony formation and reduced sphere-forming frequency from 1/33.6 to 1/68.3 cells ( = 0.0186). These findings identify the CD6 ligand axis as a therapeutic vulnerability in BCSC-enriched TNBC and support further preclinical evaluation of CD6-directed immunotherapy as a strategy to enhance antitumor immunity while limiting tumor-initiating capacity. - Source: PubMed
Publication date: 2026/08/17
Gurrea-Rubio MikelSloan SophieChada AdityaAmarista Camila IMaeda KoheiCampbell Phillip LTsou Pei-SuenCooney Laura AWicha Max SFox David A - Chronic inflammation has long been associated with cancer initiation, yet the mechanisms linking sustained immune activation to an immune-permissive tumor microenvironment remain incompletely defined. Prevailing explanations such as immune exhaustion (IEX) or free radical mediated tissue damage, fail to account for the active state of immune tolerance, a process driven by potent negative feedback loops that systematically suppress host effector responses. - Source: PubMed
Publication date: 2026/08/11
Mazzio Elizabeth ABarnes Andrew SBadisa Ramesh BDarling-Reed Selina FSoliman Karam F A - To compare the spatiotemporal localization of Activated leukocyte cell adhesion molecule (Alcam; CD166) and Osterix (OSX), encoded by Sp7, an established odontoblast differentiation marker, during rat molar development using immunohistochemical approaches. - Source: PubMed
Publication date: 2026/08/09
Shibui ToruHosoya AkihiroTakahashi MasamiShibata ShunichiSeki-Kishimoto YuriTakebe HiroakiIrie Kazuharu