Author(s)

Satoru Hamada^1,2, Andrea Caballero-Benitez¹, Kate L. Duran¹, Anne M. Stevens^3,4, Thomas Spies¹, Veronika Groh^1*

¹Clinical Research Division, Fred Hutch, Seattle, WA, USA.
²Department of Pediatrics, Ryukyus University, Okinawa Prefecture, Nishihara, Japan.
³Division of Rheumatology, Department of Pediatrics, University of Washington Medicine, Seattle, WA, USA.
⁴Center for Immunity and Immuno Therapies, Seattle Children’s Research Institute, 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.

NKG2D Ligands, NKG2D⁺ CD4 T Cells, Juvenile-Onset Systemic Lupus Erythematosus, B Cells, Monocytes

Hamada, S. , Caballero-Benitez, A. , Duran, K. , Stevens, A. , Spies, T. and Groh, V. (2017) Soluble MICB in Plasma and Urine Explains Population Expansions of NKG2D⁺CD4 T Cells Inpatients with Juvenile-Onset Systemic Lupus Erythematosus. Open Journal of Immunology, 7, 1-17. doi: 10.4236/oji.2017.71001.