TY - JOUR
T1 - Immunogenetic studies of juvenile dermatomyositis. III. Study of antibody to organ‐specific and nuclear antigens
AU - Pachman, Lauren M.
AU - Friedman, Jan M.
AU - Maryjowski‐Sweeney, Mona L.
AU - Jonnason, Olga
AU - Radvany, Ruta M.
AU - Sharp, Gordon C.
AU - Cobb, Mike A.
AU - Battles, Norma D.
AU - Crowe, William E.
AU - Fink, Chester W.
AU - Hanson, Virgil
AU - Levinson, Joseph E.
AU - Spencer, Charles H.
AU - Sullivan, Donita B.
PY - 1985/2
Y1 - 1985/2
N2 - Ninety children with definite juvenile dermatomyositis (JDMS), who had been HLA typed, were tested for the presence of tissue or organ‐specific antibodies. Sixty had active disease at the time of study. The mean disease duration was 4 years, and 30 had soft tissue calcifications. The following autoantibodies were sought: thyroid, gastric parietal cells, smooth muscle, striated muscle, microsomes, mitochondria, DNA, extractable nuclear antigen, Sm, PM‐1, antinuclear antibody (ANA), and rheumatoid factor. Only the ANA and PM‐1 were more frequent in patients than in controls (P < 0.0002 and P < 0.001, respectively). Higher levels of immune complexes (P < 0.01) were found in sera from patients with JDMS than in sera from controls and were correlated with the presence of ANA in patients (P < 0.01). Soft tissue calcification was not associated with any autoantibody or HLA antigen, but with disease duration and activity (P < 0.001 and P < 0.05, respectively). There was no association between the occurrence of any autoantibody and the presence of HLA‐B8 or DR3 among the white patients with JDMS. The frequency of autoantibodies in 43 full siblings of children with JDMS was not increased. We conclude that children with JDMS, with or without HLA‐B8/DR3, do not show evidence of a generalized nonspecific antibody response to tissue antigens. The significance of the increased antibody to nuclear antigens ANA and PM‐1 remains to be determined.
AB - Ninety children with definite juvenile dermatomyositis (JDMS), who had been HLA typed, were tested for the presence of tissue or organ‐specific antibodies. Sixty had active disease at the time of study. The mean disease duration was 4 years, and 30 had soft tissue calcifications. The following autoantibodies were sought: thyroid, gastric parietal cells, smooth muscle, striated muscle, microsomes, mitochondria, DNA, extractable nuclear antigen, Sm, PM‐1, antinuclear antibody (ANA), and rheumatoid factor. Only the ANA and PM‐1 were more frequent in patients than in controls (P < 0.0002 and P < 0.001, respectively). Higher levels of immune complexes (P < 0.01) were found in sera from patients with JDMS than in sera from controls and were correlated with the presence of ANA in patients (P < 0.01). Soft tissue calcification was not associated with any autoantibody or HLA antigen, but with disease duration and activity (P < 0.001 and P < 0.05, respectively). There was no association between the occurrence of any autoantibody and the presence of HLA‐B8 or DR3 among the white patients with JDMS. The frequency of autoantibodies in 43 full siblings of children with JDMS was not increased. We conclude that children with JDMS, with or without HLA‐B8/DR3, do not show evidence of a generalized nonspecific antibody response to tissue antigens. The significance of the increased antibody to nuclear antigens ANA and PM‐1 remains to be determined.
UR - http://www.scopus.com/inward/record.url?scp=0021955594&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0021955594&partnerID=8YFLogxK
U2 - 10.1002/art.1780280208
DO - 10.1002/art.1780280208
M3 - Article
C2 - 3871616
AN - SCOPUS:0021955594
VL - 28
SP - 151
EP - 157
JO - Arthritis and Rheumatology
JF - Arthritis and Rheumatology
SN - 2326-5191
IS - 2
ER -