The mechanism of selective anti-hapten IgE antibody production was studied in SJL mice. Using an adoptive transfer method of spleen cells into syngeneic recipients irradiated with a sublethal dose of 600 rads, it was demonstrated that for the suppression of anti-dinitrophenyl (DNP) IgE antibody production the interaction of two subsets of T cells is necessary. DNP-primed B cells and carrier-primed T helper cells are taken from donors primed with small amounts of DNP-carrier conjugates. Without injection of other cells, high titer and persistent anti-DNP antibodies are produced in the recipients. The two subsets of T cells that are active in suppression of IgE are taken from two types of donors: one donor is immunized (hyperprimed) with larger amounts of carrier protein twice, the other is an unprimed donor. The carrier for hyperpriming the first type of donor may be unrelated to the carrier used for priming the helper T cells. To bring about anti-DNP IgE suppression it is necessary that the animals should be challenged with the same DNP-carrier conjugate used for priming the B and T helper cells. If the hyperprimed donors were immunized with a heterologous, unrelated carrier, then this heterologous unconjugated carrier must also be injected together with the homologous DNP-carrier conjugate. In these conditions, anti-DNP IgE antibody production is suppressed, but the production of anti-DNP IgG1 antibody is not diminished.
Effects of administration of various adjuvants were examined for the induction of IgE antibody response against a hapten-carrier conjugate in the mouse. It was confirmed that alum was an excellent adjuvant for induction of IgE antibody response, while poly A:U, CFA and LPS had much less activity. However, when these adjuvants were administered before immunization with antigen and alum, they suppressed the forthcoming antibody response to various degrees. Even alum exerted a profound suppressive effect when it was given before immunization. Such suppressive effect of alum and poly A:U was partially overcome by incorporating in the adjuvant the carrier protein. In contrast the suppressive effect of CFA was overcome by incorporating in the CFA an unrelated carrier conjugated to the same hapten (DNP). The results indicate that the target of the adjuvants is different from one to the other and further give a clue to study the possible application for the suppression of IgE antibody formation.
The anti-IgE autoantibody in the IgG class was detected in 95.5% of patients with atopic asthma, and in 72.2% of those with non-atopic asthma, using a newly established solid phase enzyme immunoassay (EIA). The specificity of anti-IgE autoantibody was confirmed by both competitive inhibition and absorption experiments, using human IgG, IgA, IgM, IgD, IgE and rabbit anti-human IgG. Significant correlations were observed between the levels of the anti-IgE autoantibody and the serum IgE. Gel filtration studies indicated that the anti-IgE autoantibody in sera from asthmatic patients was present in the immune complex form with self-IgE, in addition to the monomeric antibody. Furthermore, this anti-IgE autoantibody has the ability to induce the reversed type immediate skin reaction, in asthma free individuals. These observations strongly suggest the putative role of the anti-IgE autoantibody in the modulation of IgE-mediated immune systems and the pathogenesis of bronchial asthma.
Research Articles| July 30 2009 In vitro Production of Anti-mite IgE Antibody and Its Suppression by Human Peripheral Blood Lymphocytes Subject Area: Immunology and Allergy I. Iwamoto; I. Iwamoto Second Department of Internal Medicine, School of Medicine, Chiba University, Chiba, Japan Search for other works by this author on: This Site PubMed Google Scholar Y. Nawata; Y. Nawata Second Department of Internal Medicine, School of Medicine, Chiba University, Chiba, Japan Search for other works by this author on: This Site PubMed Google Scholar T. Yanagisawa; T. Yanagisawa Second Department of Internal Medicine, School of Medicine, Chiba University, Chiba, Japan Search for other works by this author on: This Site PubMed Google Scholar S. Yoshida; S. Yoshida Second Department of Internal Medicine, School of Medicine, Chiba University, Chiba, Japan Search for other works by this author on: This Site PubMed Google Scholar T. Itaya; T. Itaya Second Department of Internal Medicine, School of Medicine, Chiba University, Chiba, Japan Search for other works by this author on: This Site PubMed Google Scholar H. Tomioka; H. Tomioka Second Department of Internal Medicine, School of Medicine, Chiba University, Chiba, Japan Search for other works by this author on: This Site PubMed Google Scholar A. Kumagai A. Kumagai Second Department of Internal Medicine, School of Medicine, Chiba University, Chiba, Japan Search for other works by this author on: This Site PubMed Google Scholar International Archives of Allergy and Applied Immunology (1981) 66 (Suppl. 1): 67–74. https://doi.org/10.1159/000232872 Article history Published Online: July 30 2009 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation I. Iwamoto, Y. Nawata, T. Yanagisawa, S. Yoshida, T. Itaya, H. Tomioka, A. Kumagai; In vitro Production of Anti-mite IgE Antibody and Its Suppression by Human Peripheral Blood Lymphocytes. International Archives of Allergy and Applied Immunology 1 January 1981; 66 (Suppl. 1): 67–74. https://doi.org/10.1159/000232872 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsInternational Archives of Allergy and Applied Immunology Search Advanced Search Article PDF first page preview Close Modal This content is only available via PDF. 1981Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements. You do not currently have access to this content.
