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From the Departments of Neurology (Drs. Brod and Wolinsky and Mr. Khan) and Internal Medicine (Dr. Marshall and Mrs. Henninger), University of Texas-Houston, Health Science Center, Houston, TX; and the Department of Neurology (Dr. Sriram), Vanderbilt Stallworth Research Hospital, Nashville, TN.
Supported in part by a grant from the Clayton Foundation.
Received March 22, 1995. Accepted in final form September 29, 1995.
Address correspondence and reprint requests to Dr. Staley A. Brod, University of Texas Health Science Center at Houston, Department of Neurology, 7.044, P.O. Box 20708, Houston, TX 77225.
MS is presumed to be a T-cell-mediated chronic inflammatory disease of the CNS. We examined proliferation and cytokine secretion of mononuclear cells after stimulation with OKT3 [anti-CD3] monoclonal antibody (MAb) or concanavalin A (Con A) in subjects with stable relapsing-remitting MS (RR MS) before and after initiating interferon (IFN)-beta1b treatment. There was no significant difference in pretreatment to on-treatment anti-CD3 mAb or Con A-induced proliferation in RR MS patients. There was significantly increased Con A-induced secretion of tumor necrosis factor (TNF)-alpha, IFN-gamma, interleukin (IL)-2, IL-6, and IL-10 and decreased IL-4 secretion in on-treatment compared with pretreatment peripheral blood mononuclear cell samples. However, on-treatment CD3-mediated secretion of TNF-alpha was significantly decreased, and IL-6 secretion was significantly increased compared with pretreatment values. IFN-gamma was also decreased in on-treatment cultures stimulated with anti-CD3 MAb, but these values did not reach statistical significance. Systemic side effects from IFN-beta1b were associated with increased IL-6 secretion. There were no significant changes in CD3-mediated IL-4, IL-10, transforming growth factor (TGF)-beta, or IL-2 secretion or Con A-induced TGF-beta secretion. IFN-beta1b (Betaseron) decreases CD3-mediated TNF-alpha secretion but increases another inflammatory cytokine, IL-6, that could potentially counteract its beneficial immunomodulatory effects.
NEUROLOGY 1996;46: 1633-1638
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