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Query: UMLS:C0039483 (giant cell arteritis)
 3,204 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The analysis of the antibody repertoire of patients with giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) might identify target antigens of the autoimmune response with potential relevance to our understanding of the pathogenesis of the disease and to the development of serodiagnostic tests. To detect such antigens, we screened a cDNA library derived from normal human testis for antigens reacting with IgG antibodies in the 1 : 250 diluted sera of three patients with untreated GCA using SEREX, the serological identification of antigens by recombinant cDNA expression cloning. Of 100 000 clones screened with each serum, six, 28 and six clones, respectively, were positive, representing a total of 33 different antigens. Most of the antigens reacted only with the serum used for identification and/or at a similar frequency with normal control sera. However, lamin C and the nuclear antigen of 14 kD reacted specifically with 32% of GCA/PMR, but with none of the control sera, while human cytokeratin 15, mitochondrial cytochrome oxidase subunit II, and a new gene product were detected preferentially, but not exclusively by sera from GCA/PMR patients. We conclude that patients with GCA/PMR develop antibodies against a broad spectrum of human autoantigens. Antibodies against human lamin C, the nuclear autoantigen of 14 kD as well as human cytokeratin 15, mitochondrial cytochrome oxidase subunit II and the product of a new gene should be investigated further to determine their value as tools for the diagnosis and/or the definition of clinical subgroups of patients with GCA/PMR.
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PMID:Analysis of the B cell repertoire against autoantigens in patients with giant cell arteritis and polymyalgia rheumatica. 1187 65

Giant cell arteritis (GCA) is considered to be a T cell-dependent disease. Autoantibodies have not consistently been found in GCA. The exception is antiphospholipid antibodies (APLA), which were found in 30-80% of GCA cases. Recently, efforts have been made to seek autoantibodies in GCA using newer methods of detection: serological identification of antigens by recombinant cDNA expression cloning, and a proteomic approach. In these studies, lamin C (a nuclear envelope antigen) was recognized by antibodies in 32% of GCA sera and none of the controls. Other autoantigenic proteins were also identified: lamin A, vinculin (a cytoskeleton antigen), and annexin 5 (an endothelial protein). In a recent study, 92% of 36 patients with GCA and/or polymyalgia rheumatica (PMR) had autoantibodies to a human ferritin peptide (the heavy chain N-terminal); 89% had antibodies to bacterial ferritin peptide of Staphylococcus epidermidis. The significance of these findings needs to be studied further. GCA may be a part of the newly described ASIA syndrome (autoimmune syndrome induced by adjuvants). A recent study from Italy reported 10 cases of GCA/PMR within 3 months of influenza vaccination. These comprised 50% of all cases of GCA/PMR diagnosed during the 6 year period of the study. Another 11 cases of GCA following influenza vaccinations were reported. GCA pathogenesis involves all branches of the immune system, including antigen-presenting cells, T cells and B cells, and autoantibody formation is not uncommon. GCA etiology remains unknown, but may be associated with exposure to bacterial or viral antigens.
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PMID:Autoimmune aspects of giant cell arteritis. 2516 95