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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.
2005 (English)In: Scandinavian Journal of Immunology, 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-95034OAI: oai:DiVA.org:uu-95034DiVA: diva2:169091
Available from: 2006-11-02 Created: 2006-11-02 Last updated: 2011-06-28Bibliographically approved
In thesis
1. Early Immunostimulatory Effects of IgE- and IgG Antibodies
Open this publication in new window or tab >>Early Immunostimulatory Effects of IgE- and IgG Antibodies
2006 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Antibodies have the ability to influence their own production in a process called antibody feedback regulation. Depending on the type of antigen and the subclass of the antibody, the outcome of feedback regulation can be complete suppression or several hundred-fold enhancement of the antibody response.

IgE and IgG3 enhance responses to soluble protein antigens. Previous results suggest that IgG3-mediated enhancement of antibody responses is dependent on complement and not Fc receptors for IgG. However, the Fc receptor-deficient animals used did not completely lack the IgG3-binding FcγRI. We re-examined the role of this receptor in a new mouse strain completely lacking FcγRI and found that IgG3-mediated enhancement was unperturbed, thus confirming a role for complement.

To investigate the early responses resulting in IgE-mediated enhancement of antibody responses we used biotinylated antigen and found that mature follicular B cells and to a lesser extent transitional type 2 B cells capture IgE/antigen complexes. Adoptive transfer of CD4+ T cells expressing a transgenic TCR specific for ovalbumin demonstrated that these T cells localize near the B-cell follicle after 6-12 hours and that IgE, in contrast to IgG3, significantly increased specific T cell proliferation. After 3 days the T cells had gone through several rounds of divisions and showed an activated phenotype. Additional cell transfer studies identified CD23+ B cells as the responsible effector cells. These results indicate that the mechanism underlying IgE-mediated enhancement is rapid transport of IgE/antigen complexes by follicular B cells into B-cell follicles, followed by antigen presentation by CD23+ B cells to naïve CD4+ T cells. IgG3, inducing poor T cell responses, is more likely to depend on lowering the threshold for B-cell activation by co-ligating the B-cell receptor with the complement receptor 2/CD19 complex on the surface of the B cell.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2006. 59 p.
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 189
Immunology, Antibodies, Fc receptors, Antigen presentation, B cells, T cells, Immunologi
urn:nbn:se:uu:diva-7209 (URN)91-554-6693-1 (ISBN)
Public defence
2006-11-24, Rudbecksalen, Rudbeck Laboratory, Daghammarskölsväg 20, Uppsala, 09:15
Available from: 2006-11-02 Created: 2006-11-02Bibliographically approved

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Heyman, Birgitta
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