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Research Article Free access | 10.1172/JCI109685

Studies of T- and B-Cell Interactions in Adult Patients with Combined Immunodeficiency

T. Morito, A. D. Bankhurst, and R. C. Williams Jr.

Department of Medicine, Bernalillo County Medical Center, University of New Mexico, School of Medicine, Albuquerque, New Mexico 87131

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

Department of Medicine, Bernalillo County Medical Center, University of New Mexico, School of Medicine, Albuquerque, New Mexico 87131

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

Department of Medicine, Bernalillo County Medical Center, University of New Mexico, School of Medicine, Albuquerque, New Mexico 87131

Find articles by Williams, R. in: JCI | PubMed | Google Scholar

Published February 1, 1980 - More info

Published in Volume 65, Issue 2 on February 1, 1980
J Clin Invest. 1980;65(2):422–431. https://doi.org/10.1172/JCI109685.
© 1980 The American Society for Clinical Investigation
Published February 1, 1980 - Version history
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Abstract

Cellular interactions involved in the pathogenesis of hypogammaglobulinemia were studied in six patients with common variable immunodeficiency. Amounts of immunoglobulin (Ig)G and IgM in the supernate of pokeweed mitogen-stimulated cocultures of normal and immunodeficient mononuclear cells were measured by radioimmunoassays. Mononuclear cells from three of six patients inhibited Ig production of normal B cells (P < 0.005). When purified patient and normal T cells were added to B cells in various autologous or allogeneic combinations, it was observed that immunodeficient T cells (AT) from four patients suppressed normal IgM synthesis. Allogeneic normal T cells did not provide help for B cells from these same immunodeficient patients. In two patients, autologous T cells were able to help autologous B-cell IgM synthesis in vitro. In five patients, AT cells inhibited normal B-cell IgG synthesis. Removal of T cells bearing Ia determinants or T cells with Fc-IgG receptors did not diminish the suppressive effect of AT cells on normal B-cell Ig synthesis. Addition of indomethacin, a prostaglandin synthetase inhibitor, did not abrogate the suppressive effect of immunodeficient mononuclear cells. Addition of hydrocortisone succinate (10 μM) did reverse the suppressive effect of AT cells on IgM production in one patient; however, no in vitro reversal of suppressor cell effect was recorded in five. Suppression by immune-deficient T cells was eliminated by 2,000 rad of x-ray irradiation in three patients. After x-ray irradiation immunedeficient T cells could function as helpers of normal B cells.

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