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
- Endophilin A3-mediated clathrin-independent endocytosis (EndoA3-mediated CIE) contributes to the internalization of immunoglobulin-like proteins, including key immune synapse components. Here, we identify ICAM1 as a novel EndoA3-dependent cargo, alongside ALCAM. We demonstrate that both proteins subsequently follow retromer-dependent retrograde transport to the -Golgi network (TGN) in cancer cells. From there, we propose that they undergo polarized redistribution to the plasma membrane, where they contribute to immune synapse formation between cancer cells and cytotoxic CD8 T cells. Disruption of EndoA3 or retromer components significantly affects the response of autologous cytotoxic CD8 T cells, as evidenced by reduced cytokine production and secretion, but increased lytic activity, while proliferation and later activation marker expression remain intact. This is accompanied by diminished ICAM1 density at the immune synapse, where we observe it arriving via polarized vesicular transport, indicating altered synapse organization. Indeed, cancer cells lacking EndoA3-mediated CIE or retromer form enlarged immune synapses that fail to sustain full T cell cytokine secretion, suggesting a compensatory attempt by T cells to overcome the defective synapse, while likely promoting more transient contacts that potentially favor serial killing. Together, these findings reveal that EndoA3-mediated CIE and retrograde transport act in concert in cancer cells to relocate immune synapse components via the Golgi, thereby fine-tuning the balance between cytotoxic T cell cytokine secretion and lytic activity. These insights contribute to a better understanding of the mechanisms governing immune synapse formation and organization, providing a necessary foundation for the long-term identification of new strategies to enhance T cell-mediated anti-tumor immunity. - Source: PubMed
Publication date: 2026/04/22
Xu ShiqiangBuridant AlixHirsch ThibaultDuhamel CélineLedoux BenjaminShafaq-Zadah MassiullahDransart EstelleThines LouiseJohannes LudgerVan der Bruggen PierreMorsomme PierreRenard Henri-François - Systemic lupus erythematosus (SLE), a complex autoimmune disease, affects multiple tissues and organs, presenting substantial challenges for both diagnosis and treatment. Both innate and adaptive immune cells are involved in the intricate pathophysiology of SLE. The characteristics of SLE include the production of autoantibodies and the formation of immune complexes that accumulate within the vasculature, leading to organ damage. Although progress in understanding the pathogenesis of SLE has lagged behind that of other autoimmune rheumatic diseases, recent findings have highlighted promising therapeutic targets and raised the prospect of personalized treatment strategies. This narrative review was conducted through a comprehensive analysis of recent literature focused on the pathogenesis, diagnosis, and treatment of SLE. Prospective experimental and clinical studies with well-documented results were selected for analysis. Diagnostic biomarkers were evaluated for their sensitivity, specificity, and correlation with disease activity indices, such as the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). Therapeutic agents, including monoclonal antibodies, interferon, and interleukin inhibitors, as well as emerging small molecules, were assessed based on clinical trial outcomes and potential future applicability in clinical practice. Several promising biomarkers, such as pentraxin 3 (PTX3), S100 calcium-binding protein A8 (S100A8), B cell differentiation factor (BCDF), interferon gamma-induced protein 10 (IP-10), urinary activated leukocyte cell adhesion molecule (ALCAM), vascular cell adhesion molecule 1 (VCAM-1), and platelet factor 4 (PF4), have shown strong correlations with disease activity and lupus nephritis (LN). Among treatments, monoclonal antibodies, such as belimumab and anifrolumab, are already approved by the United States Food and Drug Administration. Meanwhile, others, including obinutuzumab and sifalimumab, have demonstrated encouraging results in Phase II trials. These developments reflect growing potential for precision diagnostics and targeted therapy in SLE. Recent advances in understanding the immunological underpinnings of SLE have led to the identification of sensitive and specific biomarkers, as well as novel biologics, which may overcome the limitations of traditional therapies. Biomarkers such as PTX3 and S100A8 can facilitate early diagnosis and may also predict treatment efficacy, offering the foundation for tailored therapeutic strategies. The continued evaluation of emerging biologics, particularly those targeting B cells and the interferon pathway, holds promise for enhancing disease management and improving long-term patient outcomes. - Source: PubMed
Blagov AlexanderKalmykov VladislavAsoyan AlikhanMaltseva OlgaOrekhov Alexander - The early and accurate diagnosis of acute myocardial infarction (AMI) remains a significant clinical challenge. To this end, we profiled the surface proteome of individual plasma extracellular vesicles (EVs) from AMI patients using single-vesicle sequencing, aiming to identify disease-associated alterations with diagnostic and therapeutic potential. Profiling the EV surface proteome across healthy controls (HC), coronary artery stenosis (CAS), and AMI revealed 21 differentially expressed proteins (DEPs), 11 of which were uniquely associated with AMI compared to HC. Notably, these included elevated levels of DSCAML1, CR1, ACE2, FN1, CDH15, and C5b‑9. EVs were subsequently stratified into 17 subpopulations, with clusters 1, 8, and 9 characterized by DSCAML1, ALCAM, and CR1, respectively, and showing the highest enrichment in AMI. We further demonstrated that plasma EVs from AMI patients (AMI-EVs) promote cardiomyocyte proliferation and endothelial cell activity in vitro, followed by the finding that the DSCAML1-enriched subpopulation (DSCAML1-EVs) enhances myocardial repair and angiogenesis both in vitro and in vivo, with mechanistic studies implicating the EREG/ERK pathway in these effects. In summary, DSCAML1-positive EVs show dual potential as both a diagnostic biomarker for AMI and a therapeutic target for improving post‑infarction prognosis, providing insight into the translational potential of EV‑based strategies in precision cardiology. - Source: PubMed
Publication date: 2026/03/23
Liu NanWei GuoyueWang HaoranZhang YamengSun XipengLai FenglingZheng YanHu KeqingXu TaoSu GuohaiHuang RongTong Lingjun - Ménière's disease (MD) is a complex disorder whose pathogenesis extends beyond endolymphatic hydrops to involve dysregulated immune responses. While a subset of patients exhibits a "low-cytokine phenotype" during remission, the mechanisms underlying the transition to acute inflammatory attacks triggered by environmental factors remain poorly understood. - Source: PubMed
Publication date: 2026/03/06
Peng LuZhu BoyuLi YongpengLan YingZhan XiaolinPan XiaoLi ShiliaoYin Shihua - Endometriosis (EMS) is characterized by pain symptoms that seriously affect patients' quality of life. Gut microbiome-related metabolites (GMRM) play an important role in the process of EMS. However, the role of GMRM in endometrial stem cells and EMS-related pain remains unclear. - Source: PubMed
Publication date: 2026/02/17
Shi WenWang MinyiJin ZhuangChen XiaochuanLi JinboLai HuilingLi XiaoZhong QiyuChen YeChen Shuqin