PubMed:22215667 JSONTXT

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of antigen trafficking through scavenger receptor A.\nB 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."}

{"project":"mondo_disease","denotations":[{"id":"T1","span":{"begin":1419,"end":1437},"obj":"Disease"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MONDO_0007179"}],"text":"Inhibition of antigen trafficking through scavenger receptor A.\nB 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."}

{"project":"GlyCosmos15-HP","denotations":[{"id":"T1","span":{"begin":189,"end":201},"obj":"Phenotype"},{"id":"T2","span":{"begin":315,"end":327},"obj":"Phenotype"},{"id":"T3","span":{"begin":1247,"end":1251},"obj":"Phenotype"},{"id":"T4","span":{"begin":1419,"end":1437},"obj":"Phenotype"}],"attributes":[{"id":"A1","pred":"hp_id","subj":"T1","obj":"HP:0002960"},{"id":"A2","pred":"hp_id","subj":"T2","obj":"HP:0002960"},{"id":"A3","pred":"hp_id","subj":"T3","obj":"HP:0001644"},{"id":"A4","pred":"hp_id","subj":"T4","obj":"HP:0002960"}],"namespaces":[{"prefix":"HP","uri":"http://purl.obolibrary.org/obo/HP_"}],"text":"Inhibition of antigen trafficking through scavenger receptor A.\nB 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."}

{"project":"NCBITAXON","denotations":[{"id":"T1","span":{"begin":42,"end":51},"obj":"OrganismTaxon"},{"id":"T2","span":{"begin":240,"end":249},"obj":"OrganismTaxon"},{"id":"T3","span":{"begin":884,"end":889},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"30848"},{"id":"A2","pred":"db_id","subj":"T2","obj":"30848"},{"id":"A3","pred":"db_id","subj":"T3","obj":"9606"}],"text":"Inhibition of antigen trafficking through scavenger receptor A.\nB 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."}

{"project":"Anatomy-UBERON","denotations":[{"id":"T1","span":{"begin":64,"end":70},"obj":"Body_part"},{"id":"T2","span":{"begin":299,"end":305},"obj":"Body_part"},{"id":"T3","span":{"begin":357,"end":394},"obj":"Body_part"},{"id":"T4","span":{"begin":403,"end":414},"obj":"Body_part"},{"id":"T5","span":{"begin":425,"end":440},"obj":"Body_part"},{"id":"T6","span":{"begin":442,"end":445},"obj":"Body_part"},{"id":"T7","span":{"begin":519,"end":525},"obj":"Body_part"},{"id":"T8","span":{"begin":544,"end":547},"obj":"Body_part"},{"id":"T9","span":{"begin":591,"end":594},"obj":"Body_part"},{"id":"T10","span":{"begin":1161,"end":1167},"obj":"Body_part"},{"id":"T11","span":{"begin":1240,"end":1246},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/CL_0000236"},{"id":"A2","pred":"uberon_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/CL_0000236"},{"id":"A3","pred":"uberon_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/CL_0000145"},{"id":"A4","pred":"uberon_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/CL_0000235"},{"id":"A5","pred":"uberon_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/CL_0000451"},{"id":"A6","pred":"uberon_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/CL_0000451"},{"id":"A7","pred":"uberon_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/CL_0000236"},{"id":"A8","pred":"uberon_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/CL_0000451"},{"id":"A9","pred":"uberon_id","subj":"T9","obj":"http://purl.obolibrary.org/obo/CL_0000451"},{"id":"A10","pred":"uberon_id","subj":"T10","obj":"http://purl.obolibrary.org/obo/CL_0000084"},{"id":"A11","pred":"uberon_id","subj":"T11","obj":"http://purl.obolibrary.org/obo/CL_0000236"}],"text":"Inhibition of antigen trafficking through scavenger receptor A.\nB 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."}

{"project":"Glycosmos15-CL","denotations":[{"id":"T1","span":{"begin":64,"end":70},"obj":"Cell"},{"id":"T2","span":{"begin":299,"end":305},"obj":"Cell"},{"id":"T3","span":{"begin":354,"end":394},"obj":"Cell"},{"id":"T4","span":{"begin":403,"end":414},"obj":"Cell"},{"id":"T6","span":{"begin":425,"end":440},"obj":"Cell"},{"id":"T8","span":{"begin":442,"end":445},"obj":"Cell"},{"id":"T9","span":{"begin":519,"end":525},"obj":"Cell"},{"id":"T10","span":{"begin":544,"end":547},"obj":"Cell"},{"id":"T11","span":{"begin":580,"end":587},"obj":"Cell"},{"id":"T12","span":{"begin":591,"end":594},"obj":"Cell"},{"id":"T13","span":{"begin":1081,"end":1088},"obj":"Cell"},{"id":"T14","span":{"begin":1161,"end":1167},"obj":"Cell"},{"id":"T15","span":{"begin":1240,"end":1246},"obj":"Cell"}],"attributes":[{"id":"A1","pred":"cl_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/CL:0000236"},{"id":"A2","pred":"cl_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/CL:0000236"},{"id":"A3","pred":"cl_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/CL:0000145"},{"id":"A4","pred":"cl_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/CL:0000235"},{"id":"A5","pred":"cl_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/CL:0000394"},{"id":"A6","pred":"cl_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/CL:0000451"},{"id":"A7","pred":"cl_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/CL:0001056"},{"id":"A8","pred":"cl_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/CL:0000451"},{"id":"A9","pred":"cl_id","subj":"T9","obj":"http://purl.obolibrary.org/obo/CL:0000236"},{"id":"A10","pred":"cl_id","subj":"T10","obj":"http://purl.obolibrary.org/obo/CL:0000451"},{"id":"A11","pred":"cl_id","subj":"T11","obj":"http://purl.obolibrary.org/obo/CL:0000236"},{"id":"A12","pred":"cl_id","subj":"T12","obj":"http://purl.obolibrary.org/obo/CL:0000451"},{"id":"A13","pred":"cl_id","subj":"T13","obj":"http://purl.obolibrary.org/obo/CL:0000236"},{"id":"A14","pred":"cl_id","subj":"T14","obj":"http://purl.obolibrary.org/obo/CL:0000084"},{"id":"A15","pred":"cl_id","subj":"T15","obj":"http://purl.obolibrary.org/obo/CL:0000236"}],"text":"Inhibition of antigen trafficking through scavenger receptor A.\nB 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."}