Groh, V., Bruhl, A., El-Gabalawy, H., Nelson, J.L. and Spies, T. (2003) Stimulation of T Cell Autoreactivity by Anomalous Expression of NKG2D and Its MIC Ligands in Rheumatoid Arthritis. Proceedings of the National Academy of Sciences, 100, 9452-9457.
https://doi.org/10.1073/pnas.1632807100

has been cited by the following article:

• TITLE: Soluble MICB in Plasma and Urine Explains Population Expansions of NKG2D+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

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

  JOURNAL NAME: Open Journal of Immunology, Vol.7 No.1, March 29, 2017

  ABSTRACT: 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.