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Free access | 10.1172/JCI109396

Studies of Immune Functions of Patients with Systemic Lupus Erythematosus: COMPLEMENT-DEPENDENT IMMUNOGLOBULIN M ANTI-THYMUS-DERIVED CELL ANTIBODIES PREFERENTIALLY INACTIVATE SUPPRESSOR CELLS

Tsuyoshi Sakane, Alfred D. Steinberg, J. Patton Reeves, and Ira Green

The Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, and Arthritis, National Institutes of Health, Bethesda, Maryland 20014

Rheumatism Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, National Institutes of Health, Bethesda, Maryland 20014

Find articles by Sakane, T. in: PubMed | Google Scholar

The Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, and Arthritis, National Institutes of Health, Bethesda, Maryland 20014

Rheumatism Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, National Institutes of Health, Bethesda, Maryland 20014

Find articles by Steinberg, A. in: PubMed | Google Scholar

The Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, and Arthritis, National Institutes of Health, Bethesda, Maryland 20014

Rheumatism Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, National Institutes of Health, Bethesda, Maryland 20014

Find articles by Reeves, J. in: PubMed | Google Scholar

The Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, and Arthritis, National Institutes of Health, Bethesda, Maryland 20014

Rheumatism Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, National Institutes of Health, Bethesda, Maryland 20014

Find articles by Green, I. in: PubMed | Google Scholar

Published May 1, 1979 - More info

Published in Volume 63, Issue 5 on May 1, 1979
J Clin Invest. 1979;63(5):954–965. https://doi.org/10.1172/JCI109396.
© 1979 The American Society for Clinical Investigation
Published May 1, 1979 - Version history
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Abstract

Patients with systemic lupus erythematosus (SLE) produce excessive amounts of autoantibodies. It has also been demonstrated in several systems that such patients have a relative loss of suppressor thymus-derived (T) cells that inhibit the immune response. This loss of suppressor cells has been suggested as one of the causes of the excessive production of antibodies in patients with SLE.

In the present report we have tested the hypothesis that anti-T-cell antibodies found in the plasma of some patients with SLE preferentially kill suppressor cells. T cells from normal individuals can be activated by concanavalin A to develop suppressor cell activity. We therefore cultured normal T cells together with concanavalin A in the presence of plasma or plasma fractions from patients with SLE. We found that plasma from patients with active SLE, in which anti-T-cell antibodies were present, inhibited the development of suppressor activity in such cultures. In contrast, plasma from other active patients and patients with inactive SLE, in which no anti-T-cell antibodies could be detected, failed to block the development of such suppressor activity. Absorption of the plasma that contained anti-T-cell antibodies with T cell, but not non-T cells, could eliminate the suppressor-inhibiting activity of the SLE plasma that contained anti-T-cell antibodies. The immunoglobulin (Ig)M, but not the IgG, fraction of the plasma was shown to possess the inhibiting property and complement was found to be necessary for the effect of such anti-T-cell antibodies. We also demonstrated that exposure of normal T cells to such anti-T-cell antibodies and complement did not affect another population of T cells that could proliferate in response to mitogens.

Thus, certain patients with SLE have in their plasma an antibody of the IgM class that can selectively eliminate a population of T cells capable of developing suppressor function. The loss of suppressor T cells in patients with SLE may be the result of the effects of such antibody activity in vivo.

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