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Autoantibodies to glutathione S-transferase theta 1 in patients with primary sclerosing cholangitis and other autoimmune diseases.

Journal article
Authors Brita Ardesjö
Caisa M Hansson
Carl E G Bruder
Fredrik Rorsman
Corrado Betterle
Jan P Dumanski
Olle Kämpe
Olov Ekwall
Published in Journal of autoimmunity
Volume 30
Issue 4
Pages 273-82
ISSN 0896-8411
Publication year 2008
Published at Institute of Clinical Sciences
Pages 273-82
Language en
Links dx.doi.org/10.1016/j.jaut.2007.11.0...
Keywords Adolescent, Adult, Aged, Aged, 80 and over, Autoantibodies, blood, Autoantigens, immunology, Autoimmune Diseases, blood, genetics, immunology, Child, Child, Preschool, Cholangitis, Sclerosing, blood, genetics, immunology, Female, Gene Library, Genotype, Glutathione Transferase, genetics, immunology, Humans, Infant, Male, Middle Aged, Oligonucleotide Array Sequence Analysis, Polymerase Chain Reaction
Subject categories Clinical immunology, Gastroenterology and Hepatology

Abstract

Primary sclerosing cholangitis (PSC) is an enigmatic disorder with a suggested autoimmune basis. A variety of autoantigens have been suggested but no specific or highly directed epitope has been identified. To address this issue, we constructed a cDNA library from normal human choledochus and screened expressing clones with serum from a patient with PSC and inflammatory bowel disease (IBD). Based on this screening, glutathione S-transferase theta 1 (GSTT1) was identified as a potential autoantigenic target. To study the specificity of GSTT1, we determined immunoreactivity using a panel of 58 patients with PSC, with and without IBD, 57 patients with IBD, 31 patients with Hashimoto's thyroiditis, 30 patients with primary biliary cirrhosis (PBC), 20 patients with insulin dependent diabetes mellitus, 22 patients with autoimmune polyendocrine syndrome type I, 10 patients with systemic lupus erythematosus (SLE), 20 patients with Sjögren's syndrome, 12 patients with autoimmune pancreatitis, 28 patients with Addison's disease, 27 patients with Grave's disease, 17 with myasthenia gravis, and 118 healthy controls. Reactivity against GSTT1 was found with PSC and IBD as well as some patients with other autoimmune pathology, indicating that this population of antibodies is neither specific nor a sensitive serologic marker for PSC, but the frequency was clearly higher in autoimmune patients than controls. GSTT1-antibodies have been described in persons with GSTT1-null genotype and are suggested to develop as an alloimmune response to blood transfusions from GSTT1-positive donors or pregnancies with GSTT1-positive children. Therefore, two IBD patients with and 15 PSC patients without GSTT1-antibodies were genotyped for GSTT1 to investigate if the presence of GSTT1-antibodies was associated with the GSTT1-null genotype and possibly caused by an alloimmune response. Both IBD patients and three of the PSC patients were of the GSTT1-null genotype. We note that the frequency of GSTT1-antibodies in this study is more than 100-fold higher than the frequency described earlier in patients with autoimmune diseases. We also observe an increased frequency of GSTT1-antibodies in patients with autoimmune diseases compared to healthy controls. This increased frequency can be explained by an autoimmune phenotype which increases susceptibility to such autoantibodies, or by a high frequency of the GSTT1-null genotype in autoimmune disease.

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