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Construction of Human Suppressor T Cell Hybridomas That Produce Glycosylation Inhibiting Factors from Peripheral Blood Mononuclear Cells of Bee Venom Sensitive Patients

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Book cover New Trends in Allergy III
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Abstract

Previous experiments on the regulation of the IgE response in BDF1 mice provided a method of generating antigen specific suppressor T cells in vitro from antigen primed T cell populations [1]. Spleen cells of BDF1 mice primed with alum absorbed ovalbumin (OVA) for a persistent IgE response produced IgE potentiating factors, i.e., glycosylated IgE binding factors (IgE-BF) after antigenic stimulation but did not contain antigen-specific suppressor cells [2]. However, propagation of the antigen-activated T cells by interleukin-2 (IL-2) in the presence of glycosylation inhibiting factor (GIF) [3] or synthetic phospholipase A2 inhibitor facilitated the generation of antigen specific T cells that produced their own GIF. Stimulation of the T cells with OVA-pulsed syngeneic macrophages resulted in the formation of an IgE suppressive factor, i.e., unglycosylated IgE-BF and GIF, the latter of which had affinity for OVA. Thus, T cell hybridomas were constructed from the OVA specific T cells. Upon antigenic stimulation, some of the hybridomas formed OVA-binding GIF, which suppressed the primary IgE response of BDF 1 mice to dinitrophenol (DNP)-OVA in a carrier specific manner [4] and which shared common antigenic structures with effector type, antigen specific, suppressor T cell factor (TseF) [5].

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© 1991 Springer-Verlag Berlin Heidelberg

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Thomas, P., Carini, C., Iwata, M., Ishizaka, K. (1991). Construction of Human Suppressor T Cell Hybridomas That Produce Glycosylation Inhibiting Factors from Peripheral Blood Mononuclear Cells of Bee Venom Sensitive Patients. In: Ring, J., Przybilla, B. (eds) New Trends in Allergy III. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-46717-2_14

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  • DOI: https://doi.org/10.1007/978-3-642-46717-2_14

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-46719-6

  • Online ISBN: 978-3-642-46717-2

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