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Research Article Free access | 10.1172/JCI110104

Dysfunctions of Pokeweed Mitogen-stimulated T and B Lymphocyte Responses Induced by Gammaglobulin Therapy

Anne Durandy, Alain Fischer, and Claude Griscelli

Groupe d'Immunologie et Rhumatologie Pédiatriques, Institut National de la Santé et de la Recherche Medicale U 132, Paris, Cedex 75730, France

Department of Pediatrics, Hôpital des Enfants Malades, Paris, Cedex 75730, France

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

Groupe d'Immunologie et Rhumatologie Pédiatriques, Institut National de la Santé et de la Recherche Medicale U 132, Paris, Cedex 75730, France

Department of Pediatrics, Hôpital des Enfants Malades, Paris, Cedex 75730, France

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

Groupe d'Immunologie et Rhumatologie Pédiatriques, Institut National de la Santé et de la Recherche Medicale U 132, Paris, Cedex 75730, France

Department of Pediatrics, Hôpital des Enfants Malades, Paris, Cedex 75730, France

Find articles by Griscelli, C. in: PubMed | Google Scholar

Published March 1, 1981 - More info

Published in Volume 67, Issue 3 on March 1, 1981
J Clin Invest. 1981;67(3):867–877. https://doi.org/10.1172/JCI110104.
© 1981 The American Society for Clinical Investigation
Published March 1, 1981 - Version history
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Abstract

Lymphocytes obtained from nonimmuno deficient children treated with commercially available preparations of gammaglobulin failed to proliferate and to mature into plasma cells in vitro after stimulation with pokeweed mitogen. The influence of the treatment on lymphocyte functions varied according to the cell population considered. A T helper cell activity was detected in these patients but only in the cell subset bearing receptors for IgG after irradiation. T lymphocytes exerted a suppressive effect that disappeared after irradiation or incubation at 37°C. The suppressive cells were found among E rosette-forming cells depleted of leukocytes bearing receptors for IgG. Their suppressive effect was expressed only in the presence of normal radioresistant T lymphocytes that did not bear Fc receptors for IgG. Similar dysfunctions could be induced in vitro by incubation of normal T and B lymphocytes with gammaglobulin preparations. Because F(ab)′2 fragments or deaggregated preparations of gammaglobulin failed to activate T suppressor lymphocytes, this activation was likely triggered by attachment of Fc portion of denatured IgG to the corresponding membrane receptor. This activation step was prostaglandin E2-dependent, suggesting that activated monocytes were involved in the activation process. B lymphocyte responses appeared directly inhibited by attachment of denatured gammaglobulin on membrane Fc receptor. Our observations suggest that immunological effects of gammaglobulin therapy are not limited to antibody transfer, since it also induces subtle modifications of in vitro pokeweed mitogen-stimulated T and B cell responses. These modifications must be considered in interpreting results obtained in immunodeficient patients investigated under gamma-globulin therapy.

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