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.