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Lymphocytes Causing Their Deletion and the Abrogation of Suppressor Function1
From the Department of Immunology and Rheumatology, Instituto Nacional de la Nutrición, México 22, D. F., México
Abstract
We have previously shown that an anti-ribonucleoprotein (RNP) IgG can penetrate into live human mononuclear cells (MNC) having receptors for the Fc portion of IgG. Because T cells with such receptors (T cells) seem to behave as suppressor cells in immune regulation and because this suppressor function is diminished in diseases where antinuclear antibodies appear, we considered the possibility that antinuclear IgG antibody could penetrate T cells and affect them.
Herein we show that fluorescein-labeled anti-RNP IgG can penetrate into T cells, enriched by either mitogenic stimulation or separation with a subpopulation of T cells with low affinity for sheep erythrocytes. Incubation of MNC with anti-RNP IgG before carrying out the separation procedures resulted in apparent loss of T cells at the end of separation. To confirm that deletion had actually occurred, we performed a cytotoxicity assay using 51Cr-labeled T cells. Anti-RNP IgG had a significantly higher cytotoxic effect than normal IgG on T cells, particularly on those with low affinity for sheep erythrocytes that include most T cells.
Suppressor cell function studied in a system where it was expanded, by either 7-day culture or incubation with concanavalin A, and detected in a reverse plaque-forming cell assay with rabbit anti-human immunoglobulin-developing antibody was found to be abrogated by the addition of anti-RNP IgG to the suppressor function-expanding cultures.
Controls in Ig-free medium, or medium supplemented with normal human IgG, aggregated normal human IgG, BSA-anti-BSA immune complexes, or F(ab')2 fragments of the anti-RNP IgG, did not abrogate suppressor cell function. This indicates that the abrogation of suppressor cell function by anti-RNP IgG is due to its penetration into T cells. Suppressor cell loss and/or dysfunction caused by penetration of antinuclear antibodies into T cells may lead to the self-perpetuation of autoimmune disease.
Footnotes
1 This work was supported by Grant 1485 from the Programa Nacional de Salud, Consejo Nacional de Ciencia y Tecnología, México, and grants from the Fondo de Fomento Educativo, the Academia Nacional de Medicina, and the Mary Street Jenkins Foundation, México.
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