ANTICYTOSKELETAL AUTOANTIBODY DEVELOPMENT IN ADJUVANT ARTHRITIS

Citation
A. Franch et al., ANTICYTOSKELETAL AUTOANTIBODY DEVELOPMENT IN ADJUVANT ARTHRITIS, Journal of rheumatology, 21(3), 1994, pp. 489-497
Citations number
47
Categorie Soggetti
Rheumatology
Journal title
ISSN journal
0315162X
Volume
21
Issue
3
Year of publication
1994
Pages
489 - 497
Database
ISI
SICI code
0315-162X(1994)21:3<489:AADIAA>2.0.ZU;2-8
Abstract
Objective. Because the presence of autoantibodies against cell compone nts is a common feature of most autoimmune diseases and some of these autoantibodies have been detected in sera of patients with rheumatic d iseases such as rheumatoid arthritis (RA), we studied the presence of autoantibodies to cell components in an experimental model of chronic inflammation in rats, adjuvant arthritis (AA), to determine possible s imilarities between AA and human RA. Methods. Sera from arthritic rats were initially tested by indirect immunofluorescence using rat liver sections as a substrate. Afterwards, arthritis sera were further studi ed in cultures of human skin fibroblasts and the HEp-2 cell line, with or without colchicine treatment. Results. Results using liver as subs trate showed that 31% of the arthritic rats showed a cytoskeleton stai ning pattern throughout the cytoplasm, with higher intensity of staini ng along the surface membranes, particularly in pericanalicular region s. This staining was suggestive of intermediate filament autoantibodie s. When sera were analyzed on cultured cells, the results showed that the pattern is identical to the arrangement described for intermediate filaments and different from those seen with antiactin antibodies. Co lchicine pretreatments ruled out antitubulin activity. Further analysi s by immunoblotting revealed that autoantibodies did not recognize int ermediate filament proteins when these were denatured in the electroph oretic process. Conclusion. The development of autoantibodies to inter mediate filament proteins, both cytokeratin and vimentin, has been dem onstrated in sera from rats with AA, in a similar manner to that descr ibed in human RA.