Soluble MICB in Plasma and Urine Explains Population Expansions of NKG2D<sup>+</sup>CD4 T Cells Inpatients with Juvenile-Onset Systemic Lupus Erythematosus — Oak Academic Publishing
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Soluble MICB in Plasma and Urine Explains Population Expansions of NKG2D<sup>+</sup>CD4 T Cells Inpatients with Juvenile-Onset Systemic Lupus Erythematosus
Clinical Research Division, Fred Hutch, Seattle, WA, USA
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Department of Pediatrics, Ryukyus University, Okinawa Prefecture, Nishihara, Japan
,
Clinical Research Division, Fred Hutch, Seattle, WA, USA
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Clinical Research Division, Fred Hutch, Seattle, WA, USA
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Division of Rheumatology, Department of Pediatrics, University of Washington Medicine, Seattle, WA, USA
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Center for Immunity and Immuno Therapies, Seattle Children’s Research Institute, Seattle, WA, USA
,
Clinical Research Division, Fred Hutch, Seattle, WA, USA
,
Clinical Research Division, Fred Hutch, Seattle, WA, USA
1 Clinical Research Division, Fred Hutch, Seattle, WA, USA
2 Department of Pediatrics, Ryukyus University, Okinawa Prefecture, Nishihara, Japan
3 Clinical Research Division, Fred Hutch, Seattle, WA, USA
4 Clinical Research Division, Fred Hutch, Seattle, WA, USA
5 Division of Rheumatology, Department of Pediatrics, University of Washington Medicine, Seattle, WA, USA
6 Center for Immunity and Immuno Therapies, Seattle Children’s Research Institute, Seattle, WA, USA
7 Clinical Research Division, Fred Hutch, Seattle, WA, USA
8 Clinical Research Division, Fred Hutch, Seattle, WA, USA
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.
KeywordsNKG2D LigandsNKG2D<sup>+</sup>CD4 T CellsJuvenile-Onset Systemic Lupus ErythematosusB CellsMonocytes
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