Satoru Hamada, Andrea Caballero-Benitez, Kate L Duran, Anne M Stevens, Thomas Spies, Veronika Groh
{"title":"血浆和尿液中可溶性MICB解释了青少年发病系统性红斑狼疮患者NKG2D+CD4 T细胞的群体扩增。","authors":"Satoru Hamada, Andrea Caballero-Benitez, Kate L Duran, Anne M Stevens, Thomas Spies, Veronika Groh","doi":"10.4236/oji.2017.71001","DOIUrl":null,"url":null,"abstract":"<p><p>Abnormal NKG2D ligand expression has been implicated in the initiation and maintenance of various auto-inflammatory disorders including systemic lupus erythematosus (SLE). This study's goal was to identify the cellular contexts providing NKG2D ligands for stimulation of the immunosuppressive NKG2D<sup>+</sup>CD4 T cell subset that has been implicated in modulating juvenile-onset SLE disease activity. Although previous observations with NKG2D<sup>+</sup>CD4 T cells in healthy individuals pointed towards peripheral B cell and myeloid cell compartments as possible sites of enhanced NKG2DL presence, we found no evidence for a disease-associated increase of NKG2DL-positivity among juvenile-onset SLE B cells and monocytes. However, juvenile-onset SLE patient plasma and matched urine samples were positive by ELISA for the soluble form of the NKG2D ligands MICA and MICB, suggesting that kidney and/or peripheral blood may constitute the NKG2DL positive microenvironments driving NKG2D<sup>+</sup>CD4 T cell population expansions in this disease.</p>","PeriodicalId":70343,"journal":{"name":"免疫学期刊(英文)","volume":"7 1","pages":"1-17"},"PeriodicalIF":0.0000,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5604888/pdf/","citationCount":"9","resultStr":"{\"title\":\"Soluble MICB in Plasma and Urine Explains Population Expansions of NKG2D<sup>+</sup>CD4 T Cells Inpatients with Juvenile-Onset Systemic Lupus Erythematosus.\",\"authors\":\"Satoru Hamada, Andrea Caballero-Benitez, Kate L Duran, Anne M Stevens, Thomas Spies, Veronika Groh\",\"doi\":\"10.4236/oji.2017.71001\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Abnormal NKG2D ligand expression has been implicated in the initiation and maintenance of various auto-inflammatory disorders including systemic lupus erythematosus (SLE). This study's goal was to identify the cellular contexts providing NKG2D ligands for stimulation of the immunosuppressive NKG2D<sup>+</sup>CD4 T cell subset that has been implicated in modulating juvenile-onset SLE disease activity. Although previous observations with NKG2D<sup>+</sup>CD4 T cells in healthy individuals pointed towards peripheral B cell and myeloid cell compartments as possible sites of enhanced NKG2DL presence, we found no evidence for a disease-associated increase of NKG2DL-positivity among juvenile-onset SLE B cells and monocytes. However, juvenile-onset SLE patient plasma and matched urine samples were positive by ELISA for the soluble form of the NKG2D ligands MICA and MICB, suggesting that kidney and/or peripheral blood may constitute the NKG2DL positive microenvironments driving NKG2D<sup>+</sup>CD4 T cell population expansions in this disease.</p>\",\"PeriodicalId\":70343,\"journal\":{\"name\":\"免疫学期刊(英文)\",\"volume\":\"7 1\",\"pages\":\"1-17\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2017-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5604888/pdf/\",\"citationCount\":\"9\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"免疫学期刊(英文)\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.4236/oji.2017.71001\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2017/3/29 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"免疫学期刊(英文)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4236/oji.2017.71001","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2017/3/29 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
Soluble MICB in Plasma and Urine Explains Population Expansions of NKG2D+CD4 T Cells Inpatients with Juvenile-Onset Systemic Lupus Erythematosus.
Abnormal NKG2D ligand expression has been implicated in the initiation and maintenance of various auto-inflammatory disorders including systemic lupus erythematosus (SLE). This study's goal was to identify the cellular contexts providing NKG2D ligands for stimulation of the immunosuppressive NKG2D+CD4 T cell subset that has been implicated in modulating juvenile-onset SLE disease activity. Although previous observations with NKG2D+CD4 T cells in healthy individuals pointed towards peripheral B cell and myeloid cell compartments as possible sites of enhanced NKG2DL presence, we found no evidence for a disease-associated increase of NKG2DL-positivity among juvenile-onset SLE B cells and monocytes. However, juvenile-onset SLE patient plasma and matched urine samples were positive by ELISA for the soluble form of the NKG2D ligands MICA and MICB, suggesting that kidney and/or peripheral blood may constitute the NKG2DL positive microenvironments driving NKG2D+CD4 T cell population expansions in this disease.