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IgG3-mediated enhancement of the antibody response is normal in Fc gammaRI-deficient mice
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology. (Exp Immunologi)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology. (Exp Immunologi)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology. (Exp Immunologi)
2005 (English)In: Scandinavian Journal of Immunology, ISSN 0300-9475, E-ISSN 1365-3083, Vol. 62, no 5, 453-461 p.Article in journal (Refereed) Published
Abstract [en]

Antibodies, administered together with their specific antigen, can feedback-regulate antibody responses to this antigen. IgG1, IgG2a and IgG2b enhance antibody responses to soluble protein antigens. This effect is primarily mediated by FcRs as enhancement is impaired in FcR gamma-/- mice, reported to lack Fc gammaRI and Fc gammaRIII because of deletion of the common FcR gamma chain. Also IgG3 can enhance antibody responses. However, this effect is unperturbed in FcR gamma-/- mice but severely impaired in complement-depleted animals and in animals lacking complement receptor 1 and 2. Although this argues against involvement of Fc gammaRs, FcR gamma-/- mice may express one-fifth of the normal levels of Fc gammaRI and, in addition, Fc gammaRI has been suggested to bind IgG3. We re-investigated the dependence of IgG3-mediated enhancement on Fc gammaRs using a mouse strain selectively lacking Fc gammaRI and found that IgG3-mediated enhancement is completely normal. Unlike IgE and IgG2a, which are both thought to enhance T-cell proliferation via FcR-mediated antigen presentation, IgG3 was a poor enhancer of T-cell proliferation both in vivo and in vitro. These findings argue against a significant involvement of Fc gammaRs in IgG3-mediated enhancement of antibody responses and support our previous conclusion that complement plays a major role.

Place, publisher, year, edition, pages
2005. Vol. 62, no 5, 453-461 p.
Keyword [en]
Adjuvants; Immunologic/*administration & dosage/*physiology, Animals, Antibody Formation/genetics, Antigen Presentation/genetics, Antigen-Antibody Complex/administration & dosage/physiology, B-Lymphocyte Subsets/*immunology/metabolism/transplantation, CD4-Positive T-Lymphocytes/immunology/metabolism/transplantation, Epitopes; T-Lymphocyte/*immunology/metabolism, Haptens/administration & dosage/immunology, Immunoglobulin E/*administration & dosage/metabolism/*physiology, Lymphocyte Activation/genetics/immunology, Mice, Mice; Congenic, Mice; Inbred BALB C, Mice; Transgenic, Ovalbumin/administration & dosage/immunology, Receptors; IgE/*biosynthesis/deficiency/genetics, Research Support; Non-U.S. Gov't, T-Lymphocytes/*immunology/metabolism, Trinitrobenzenes/administration & dosage/immunology
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-75334DOI: 10.1111/j.1365-3083.2005.01684.xPubMedID: 16305642OAI: oai:DiVA.org:uu-75334DiVA: diva2:103244
Available from: 2006-02-06 Created: 2006-02-06 Last updated: 2017-12-14Bibliographically approved

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Hjelm, FCarlsson, FHeyman, B

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