ArticleJournal of immunology (Baltimore, Md. : 1950)2013
CD166/ALCAM mediates proinflammatory effects of S100B in delayed type hypersensitivity.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- S100B induces angiogenesis via the clathrin/FOXO1/β-catenin signaling pathway and contributes to Bevacizumab resistance in epithelial ovarian cancer.Journal of advanced research · 2026Article
- Urinary ALCAM signatures define renal activity and therapeutic response in juvenile lupus nephritis.Pediatric rheumatology online journal · 2026Article
- Serum ALCAM is a potential novel non-invasive marker for predicting the progression of IgA nephropathy.BMC nephrology · 2025Article
- Establishing a model composed of immune-related gene-modules to predict tumor immunotherapy response.Scientific reports · 2024Article
- Longitudinal assessment of urinary ALCAM, HPX, and PRDX6 in Korean patients with systemic lupus erythematosus: implications for disease activity monitoring and treatment response.Frontiers in immunology · 2024Article
- The AGE-RAGE Axis and the Pathophysiology of Multimorbidity in COPD.Journal of clinical medicine · 2023Review
- The Role of the S100 Protein Family in Glioma.Journal of Cancer · 2022Review
- Review
- S100 Proteins in Pancreatic Cancer: Current Knowledge and Future Perspectives.Frontiers in oncology · 2021Review
- The S100 Protein Family as Players and Therapeutic Targets in Pulmonary Diseases.Pulmonary medicine · 2021Review
- ALCAM and VCAM-1 as urine biomarkers of activity and long-term renal outcome in systemic lupus erythematosus.Rheumatology (Oxford, England) · 2020Article
- CD146, from a melanoma cell adhesion molecule to a signaling receptor.Signal transduction and targeted therapy · 2020Review
- Activated Leukocyte Cell Adhesion Molecule Modulates Th2 Immune Response in Atopic Dermatitis.Allergy, asthma & immunology research · 2019Article
- Inflammation: A key process in skin tumorigenesis.Oncology letters · 2019Review
- Expression profile and functional role of S100A14 in human cancer.Oncotarget · 2019Review
- ALCAM Mediates DC Migration Through Afferent Lymphatics and Promotes Allospecific Immune Reactions.Frontiers in immunology · 2019Article
- S100 proteins as therapeutic targets.Biophysical reviews · 2018Review
- Mesenchymal stem cells in peripheral blood of severely injured patients.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2018Observational
- Activated leucocyte cell adhesion molecule (ALCAM/CD166) regulates T cell responses in a murine model of food allergy.Clinical and experimental immunology · 2018Article
- The effect of lifestyle intervention in obesity on the soluble form of activated leukocyte cell adhesion molecule.BMC endocrine disorders · 2016Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Promiscuity of pattern recognition receptors, such as receptor for advanced glycation end products (RAGE), allows for a complex regulatory network controlling inflammation. Scavenging of RAGE ligands by soluble RAGE treatment is effective in reducing delayed-type hypersensitivity (DTH), even in RAGE(-/-) mice by 50% (p < 0.001). This has led to the hypothesis that molecules scavenged by soluble RAGE bind to receptors other than RAGE. This study identifies CD166/ALCAM (ALCAM) as a close structural and functional homolog of RAGE, and it shows that binding of S100B to CD166/ALCAM induces dose- and time-dependent expression of members of the NF-κB family in wild type (WT) and RAGE(-/-) mouse endothelial cells. Blocking CD166/ALCAM expression using small interfering RNA completely inhibited S100B-induced NF-κB activation in RAGE(-/-), but not in WT cells. The in vivo significance of these observations was demonstrated by attenuation of DTH in WT and RAGE(-/-) animals pretreated with CD166/ALCAM small interfering RNA by 50% and 40%, respectively (p < 0.001). Experiments in ALCAM(-/-) animals displayed an only slight reduction of 16% in DTH, explained by compensatory reciprocal upregulation of RAGE in animals devoid of CD166/ALCAM, and vice versa. Consistently, ALCAM(-/-) mice, but not WT mice treated with RAGE small interfering RNA show a 35% reduction in DTH, and ALCAM(-/-) RAGE(-/-) double-knockout mice show a 27% reduction in DTH reaction. Thus, S100B is a proinflammatory cytokine bridging RAGE and CD166/ALCAM downstream effector mechanisms, both being compensatory upregulated after genetic deletion of its counterpart.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.