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Abnormal regulation of IgG production in multiple sclerosis

Department of Basic and Clinical Immunology and Microbiology (Drs. Goust and Arnaud), and the Department of Neurology (Drs. Goust and Hogan), Medical University of South Carolina, Charleston, SC.

After stimulation with pokeweed mitogen (PWM), peripheral blood mononuclear cells (MNC) from patients with active multiple sclerosis (MS) produced significantly more IgG (8595 ng per milliliter, p < 0.01) than MNC from normal age-matched controls (5477 ng per milliliter), whereas those tested during stable periods produced less IgG (4076 ng per milliliter, p < 0.01). Treatment of MNC with sodium periodate (SP) generated suppressor cells for PWM-driven IgG production in normal controls and in most of the stable MS patients but in only 26% of those during active disease, in whom an increase in IgG production was often seen. This suggests a deficiency of inducible suppressor T cells associated with a supernormal B-cell response to polyclonal activation. T lymphocytes obtained from MS patients during active episodes strongly suppressed IgG production by normal B lymphocytes, whereas their B cells often produced more IgG in the presence of normal T cells. In active MS, a relative B-cell unresponsiveness to activated suppressor T cells would leave helper signals unbalanced, thus leading to increased B-cell activation, which might deplete the pool of inducible suppressor cells for IgG production.

Address correspondence and reprint requests to Dr. Goust, Department of Basic and Clinical Immunology and Microbiology, Medical University of South Carolina, 171 Ashley Avenue, Charleston, SC 29425.

Research supported in part by grants from the U.S. Public Health Service (NS-16269), the National Multiple Sclerosis Society, and the Owen-Cheatham Foundation.

Accepted for publication August 4, 1981.

This article has been cited by other articles:

				M. R. Mickey, G. W. Ellison, J. L. Fahey, D. J. Moody, and L. W. Myers Correlation of Clinical and Immunologic States in Multiple Sclerosis Arch Neurol, April 1, 1987; 44(4): 371 - 375. [Abstract] [PDF]