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IgG3-Mediated Enhancement of the Antibody Response is Normal in FcγRI-Deficient Mice
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Biochemistry and Microbiology.
2005 (English)In: Scandinavian Journal of Immunology, ISSN 0300-9475, Vol. 62, no 5, 453-461 p.Article in journal (Refereed) Published
Place, publisher, year, edition, pages
2005. Vol. 62, no 5, 453-461 p.
URN: urn:nbn:se:uu:diva-95524OAI: oai:DiVA.org:uu-95524DiVA: diva2:169777
Available from: 2007-03-08 Created: 2007-03-08 Last updated: 2011-06-28Bibliographically approved
In thesis
1. Antibody Feedback Regulation and T Cells
Open this publication in new window or tab >>Antibody Feedback Regulation and T Cells
2007 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Antibodies, passively administered or actively produced, regulate immune responses to the antigen they recognize. This phenomenon is called antibody-mediated feedback regulation. Feedback regulation can be positive or negative, resulting in >1000-fold enhancement or >99% suppression of the specific antibody response. The outcome depends on size, structure, dose, and route of administration of the antigen as well as on class and subclass of the regulating antibody. This thesis investigates the role of T cells in antibody-mediated feedback enhancement, using both in vivo and in vitro approaches. IgE-antibodies enhance antibody responses to small soluble proteins. This effect is entirely dependent on the low-affinity receptor for IgE, CD23, and most likely depends on increased antigen presentation by CD23+ B cells. Strengthening this hypothesis, we show that IgE-mediated CD4+ T cell proliferation in vitro required the presence of CD19+ CD43- CD23+ B cells. CD23 has also been shown to negatively regulate immune responses. Transgenic mice overexpressing CD23 are known to have impaired responses to antigens in alum. We here demonstrate that they are normal regarding IgE-mediated enhancement. IgG3 enhances antibody responses, and previous data suggested involvement of complement. We found that IgG3-mediated enhancement works well in mice lacking the only Fc-receptor known to bind IgG3, CD64. Although IgG3 could enhance antibody responses it had no major effect on T cell responses. Complement-receptors 1/2 (CR1/2) are required for the initiation of normal antibody responses. Although mice lacking CR1/2 had impaired antibody responses after immunization with sheep erythrocytes, their specific T cell responses were unaffected. The presented data do not support the idea that increased complement-mediated antigen presentation is a major mechanism behind the involvement of complement in antibody responses. They support the hypothesis that antigens forming complement-containing immune complexes may activate specific B cells by co-crosslinking BCR and CR1/2.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2007. 46 p.
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 233
Fc receptors, B cell, T cell, antigen presentation, complement receptors, complement, IgE, IgG3, CD23, antibody
National Category
Immunology in the medical area
urn:nbn:se:uu:diva-7631 (URN)978-91-554-6814-9 (ISBN)
Public defence
2007-03-30, Rudbecksalen, Rudbecklaboratoriet, Dag Hammarskölds väg 20, Uppsala, 09:15
Available from: 2007-03-08 Created: 2007-03-08Bibliographically approved

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Heyman, Birgitta
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Department of Genetics and PathologyDepartment of Medical Biochemistry and Microbiology

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