Interleukin-2 in scleroderma: correlation of serum level with extent of skin involvement and disease duration
To assess whether interleukin-2 has a role in the pathogenesis of scleroderma. Observe serum effect on the in-vitro growth of an interleukin-2-dependent cytotoxic T-cell line and determine serum level by an enzyme-linked immunosorbent assay. Outpatient rheumatology clinic of a university medical cen...
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Published in | Annals of internal medicine Vol. 110; no. 6; p. 446 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
United States
15.03.1989
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Subjects | |
Online Access | Get more information |
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Summary: | To assess whether interleukin-2 has a role in the pathogenesis of scleroderma.
Observe serum effect on the in-vitro growth of an interleukin-2-dependent cytotoxic T-cell line and determine serum level by an enzyme-linked immunosorbent assay.
Outpatient rheumatology clinic of a university medical center.
Sera were collected from 47 patients with scleroderma, 20 patients with rheumatoid arthritis, and 14 matched control subjects.
A significant mitogenic effect was observed in sera from patients with scleroderma of recent onset; a lower proliferative response was seen in rheumatoid sera. Matched control sera had no mitogenic activity. Sera from patients with scleroderma of recent onset supported the in-vitro growth of an interleukin-2-dependent cytotoxic T-cell line. Matched control sera had no similar mitogenic activity. Interleukin-2 was found in sera from 41 of 47 patients with scleroderma (204 +/- 356 U/mL, mean +/- SD), in 9 of 20 patients with rheumatoid arthritis (2.04 +/- 5.16), and in none of 14 matched control subjects. There was a positive correlation between serum level and the skin progression index (skin score/disease duration).
The presence of interleukin-2 in scleroderma sera strongly supports a role for T-cell activation in scleroderma. The association between serum levels and disease progression indicates that this T-cell process may participate in the progression of the disease. |
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ISSN: | 0003-4819 1539-3704 |
DOI: | 10.7326/0003-4819-110-6-446 |