ArticleThe Journal of biological chemistry2012
Inhibition of antigen trafficking through scavenger receptor A.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- SR-A neutralizing antibody: potential drug candidate for ameliorating osteoclastogenesis in rheumatoid arthritis.Clinical and experimental immunology · 2022Article
- Citrullination and PAD Enzyme Biology in Type 1 Diabetes - Regulators of Inflammation, Autoimmunity, and Pathology.Frontiers in immunology · 2021Review
- Pharmacology, Toxicology, and Metabolism of Sennoside A, A Medicinal Plant-Derived Natural Compound.Frontiers in pharmacology · 2021Review
- Oxidative Modifications in Tissue Pathology and Autoimmune Disease.Antioxidants & redox signaling · 2018Review
- Understanding molecular interactions between scavenger receptor A and its natural product inhibitors through molecular modeling studies.Journal of molecular graphics & modelling · 2017Article
- Design, synthesis, and characterization of rhein analogs as novel inhibitors of scavenger receptor A.Bioorganic & medicinal chemistry letters · 2017Article
- Analysis of Ebola Virus Entry Into Macrophages.The Journal of infectious diseases · 2015Article
- Small molecule inhibits activity of scavenger receptor A: Lead identification and preliminary studies.Bioorganic & medicinal chemistry letters · 2015Article
- Scavenger Receptors: Emerging Roles in Cancer Biology and Immunology.Advances in cancer research · 2015Review
- The dual role of scavenger receptor class A in development of diabetes in autoimmune NOD mice.PloS one · 2014Article
- The role of macrophage class a scavenger receptors in a laser-induced murine choroidal neovascularization model.Investigative ophthalmology & visual science · 2013Article
- Macrophage scavenger receptor 1 (Msr1, SR-A) influences B cell autoimmunity by regulating soluble autoantigen concentration.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Self double-stranded (ds)DNA induces IL-1β production from human monocytes by activating NLRP3 inflammasome in the presence of anti-dsDNA antibodies.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
B cell acquisition and presentation of specific autoantigens (auto-Ags) are thought to play an important and complex role in autoimmunity development. We previously identified scavenger receptor A (SR-A) as an early target in altering B cell-mediated autoimmunity. SR-A is highly expressed on professional antigen-presenting cells such as macrophages (MΦs) and dendritic cells (DCs). In this study, we demonstrate that SR-A is responsible for controlling B cell interactions with DCs/MΦs to promote Ag transfer from B cells to DCs/MΦs. We established a high-throughput ELISA-based screen to identify novel SR-A inhibitors, the specificity of which was determined by dose dependence and Biacore surface plasmon resonance testing. We identified small molecule inhibitors (SMIs) able to reduce SR-A-mediated Ag transfer in human cells. In particular, the SMIs prevented SR-A-positive cells from accumulating/loading Ag over time. Furthermore, we determined that one SMI, sennoside B, can reduce SR-A-mediated capture of B cells. Finally, SMI-mediated decreases in Ag transfer or accumulation reduced T cell proliferation in vitro and in vivo. These observations demonstrate that B cell-DC/MΦ interactions are conducive to promoting Ag trafficking between these cell types via SR-A. Inhibitors of SR-A may provide a novel therapeutic strategy in ameliorating autoimmune disease development.
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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.