Soluble NKG2D Ligands in Hepatic Autoimmune Diseases and in Benign Diseases Involved in Marker Metabolism

Background: Proteolytic shedding of the immunostimulatory NKG2D ligands MICA and MICB from cancer cells constitutes a novel immune escape strategy that diminishes antitumor reactivity by NKG2D-bearing cytotoxic lymphocytes. In consequence, serum levels of soluble MICA and MICB are frequently found t...

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Published in:Anticancer research 2007-07, Vol.27 (4A), p.2041-2045
Main Authors: HOLDENRIEDER, Stefan, EICHHORN, Peter, BEUERS, Ulrich, SAMTLEBEN, Walter, STIEBER, Petra, NAGEL, Dorothea, PETERFI, Andrea, STEINLE, Alexander, SALIH, Helmut Rainer
Format: Article
Language:English
Subjects:
Autoimmune Diseases - blood
Biological and medical sciences
Biomarkers - blood
Enzyme-Linked Immunosorbent Assay
Histocompatibility Antigens Class I - blood
Humans
Ligands
Liver Diseases - blood
Liver Diseases - diagnosis
Medical sciences
Nephrology. Urinary tract diseases
Nephropathies. Renovascular diseases. Renal failure
NK Cell Lectin-Like Receptor Subfamily K
Receptors, Immunologic - metabolism
Receptors, Natural Killer Cell
Renal failure
Tumors
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Summary:Background: Proteolytic shedding of the immunostimulatory NKG2D ligands MICA and MICB from cancer cells constitutes a novel immune escape strategy that diminishes antitumor reactivity by NKG2D-bearing cytotoxic lymphocytes. In consequence, serum levels of soluble MICA and MICB are frequently found to be elevated in cancer disease. Patients and Methods: As the diagnostic potential depends strongly on the organ-specific benign diseases and is affected by diseases involved in marker metabolism, both markers were analyzed by ELISA in sera of 141 patients with hepatic autoimmune diseases (34 autoimmune hepatitis, 35 primary sclerosing cholangitis, 72 primary biliary cirrhosis), 18 patients with acute bacterial infections, 21 patients with renal insufficiency, 13 patients with cholestasis and 62 healthy individuals. Results: Similarly to healthy controls (median sMICA
ISSN:0250-7005
1791-7530