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Research Article Free access | 10.1172/JCI112835

Reversal of lymphocyte activation in vivo in the Kawasaki syndrome by intravenous gammaglobulin.

D Y Leung, J C Burns, J W Newburger, and R S Geha

Find articles by Leung, D. in: JCI | PubMed | Google Scholar

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Published February 1, 1987 - More info

Published in Volume 79, Issue 2 on February 1, 1987
J Clin Invest. 1987;79(2):468–472. https://doi.org/10.1172/JCI112835.
© 1987 The American Society for Clinical Investigation
Published February 1, 1987 - Version history
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Abstract

The effect of intravenous gammaglobulin (IVGG) on the immunoregulatory abnormalities found during acute Kawasaki syndrome (KS) was studied in a randomized trial of IVGG plus aspirin (ASA) versus ASA alone. Before therapy, patients in each treatment group had increased numbers of circulating HLA-DR-bearing Leu 3+ helper T cells, a deficiency of Leu 2+ suppressor/cytotoxic T cells, and increased levels of spontaneous IgG and IgM synthesis by peripheral blood mononuclear cells. There were no significant differences (P greater than 0.1) between immunologic parameters measured on day 1 and day 4 in the ASA-treated group. In contrast, patients treated with ASA plus IVGG had by day 4 a highly significant decrease in HLA-Dr+ Leu 3+ helper T cells (P less than 0.001), an increase in Leu 2+ suppressor/cytotoxic T cells (P less than 0.01), and a decrease in spontaneous IgG (P less than 0.01) and IgM synthesis (P less than 0.001). These changes were associated with a reduction in the secretion of T cell-derived B cell helper factors (P less than 0.001). These findings indicate that treatment with IVGG suppresses the marked T and B cell activation found in patients with acute KS.

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