TY - JOUR
T1 - Cytotoxic anti‐t cell antibodies in children with juvenile rheumatoid arthritis
AU - Barron, Karyl S.
AU - Lewis, Dorothy E.
AU - Brewer, Earl J.
AU - Marcus, Donald M.
AU - Shearer, William T.
PY - 1984/11
Y1 - 1984/11
N2 - The object of this investigation was to determine the prevalence of anti‐T cell antibodies in 66 children with various connective tissue diseases. Anti‐T cell antibodies were found in 43/44 juvenile rheumatoid arthritis (JRA) patients (mean cytotoxicity 15.0%) and in 10/10 children with systemic lupus erythematosus (mean cytotoxicity 20.0%), but in only 1/15 normal controls and in none of 12 children with other arthritides. There was no significant difference in mean percent cytotoxicity among the JRA subclasses. In the JRA patients, the percent cytotoxicity was positively correlated with the erythrocyte sedimentation rate (P = 0.01), but not with the presence or absence of rheumatoid factor, antinuclear antibodies, or immune complexes. The sera of 3 JRA patients repeatedly inhibited the stimulation of normal lymphocytes by mitogens and antigens by 47–99% (measured by the incorporation of 3H‐thymidine into DNA) when added to the culture system in the first 24 hours; normal sera did not. Sera from patients with JRA have increased reactivity with mitogen‐activated lymphocytes and T cells compared with unstimulated cells as determined by flow cytometry. The expression of the “JRA antigen” requires protein synthesis but not DNA synthesis or cell division. We conclude that the majority of patients with active JRA have cytotoxic anti‐T cell antibodies and that in selected patients, these antibodies may play a role in regulation of the immune response.
AB - The object of this investigation was to determine the prevalence of anti‐T cell antibodies in 66 children with various connective tissue diseases. Anti‐T cell antibodies were found in 43/44 juvenile rheumatoid arthritis (JRA) patients (mean cytotoxicity 15.0%) and in 10/10 children with systemic lupus erythematosus (mean cytotoxicity 20.0%), but in only 1/15 normal controls and in none of 12 children with other arthritides. There was no significant difference in mean percent cytotoxicity among the JRA subclasses. In the JRA patients, the percent cytotoxicity was positively correlated with the erythrocyte sedimentation rate (P = 0.01), but not with the presence or absence of rheumatoid factor, antinuclear antibodies, or immune complexes. The sera of 3 JRA patients repeatedly inhibited the stimulation of normal lymphocytes by mitogens and antigens by 47–99% (measured by the incorporation of 3H‐thymidine into DNA) when added to the culture system in the first 24 hours; normal sera did not. Sera from patients with JRA have increased reactivity with mitogen‐activated lymphocytes and T cells compared with unstimulated cells as determined by flow cytometry. The expression of the “JRA antigen” requires protein synthesis but not DNA synthesis or cell division. We conclude that the majority of patients with active JRA have cytotoxic anti‐T cell antibodies and that in selected patients, these antibodies may play a role in regulation of the immune response.
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U2 - 10.1002/art.1780271109
DO - 10.1002/art.1780271109
M3 - Article
C2 - 6437413
AN - SCOPUS:0021716907
SN - 0004-3591
VL - 27
SP - 1272
EP - 1280
JO - Arthritis & Rheumatism
JF - Arthritis & Rheumatism
IS - 11
ER -