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Fcγ Receptors in the Immune Response
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Genetics and Pathology.
2001 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Circulating immune complexes play an important role in the modulation of antibody responses and in the pathogenesis of immune diseases. This thesis deals with the in vivo regulatory properties of antibodies and their specific Fc receptors.

The immunosuppressive function of IgG is used clinically, to prevent rhesus-negative women from becoming sensitized to rhesus-positive erythrocytes from the fetus. The mechanism behind this regulation is poorly understood but involvement of a receptor for IgG, FcγRII, has been suggested. It is shown in this thesis that IgG and also IgE induce immunosuppression against sheep erythrocytes to a similar extent both in mice lacking all the known Fc receptors as in wild-type animals. These findings imply that antibody-mediated suppression of humoral responses against particulate antigens is Fc-independent and that the major operating mechanism is masking of epitopes.

Immunization with soluble antigens in complex with specific IgG leads to an augmentation of antibody production. The cellular mechanism behind this control is examined here and it is found that the capture of IgG2a immune complexes by a bone marrow-derived cell expressing FcγRI (and FcγRIII) is essential. An analysis of the ability of IgG3 to mediate this regulation indicated that, in contrast, this subclass of IgG augments antibody responses independently of FcγRI (and FcγRIII). These findings suggest that distinct mechanisms mediate the enhancing effect of different subclasses of antibodies.

Finally, the contribution of FcγRIII was studied in the development of collagen-induced arthritis (CIA), an animal model for rheumatoid arthritis in humans. It was discovered that while DBA/1 wild-type control mice frequently developed severe CIA, with high incidence, FcγRIII-deficient mice were almost completely protected, indicating a crucial role for FcγRIII in CIA.

The results presented here help to understand how immune complexes regulate immune responses in vivo and show that Fc receptors for IgG, if involved, could be new targets for the treatment of immune complex-related disorders.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis , 2001. , p. 58
Series
Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 0282-7476 ; 1102
Keywords [en]
Genetics, Fc Receptors, IgG Receptors, IgE Receptors, Immune regulation, In vivo animal models, Mouse, Rh prophylaxis, Rheumatoid arthritis, Transgenic/knockout
Keywords [sv]
Genetik
National Category
Medical Genetics
Research subject
Pathology
Identifiers
URN: urn:nbn:se:uu:diva-1545ISBN: 91-554-5175-6 (print)OAI: oai:DiVA.org:uu-1545DiVA, id: diva2:161139
Public defence
2001-12-14, Rudbecksalen, Rudbeck Laboratory, Uppsala, 13:15
Opponent
Available from: 2001-11-23 Created: 2001-11-23 Last updated: 2018-01-13Bibliographically approved
List of papers
1. Efficient IgG-mediated suppression of primary antibody responses in Fcgamma receptor-deficient mice
Open this publication in new window or tab >>Efficient IgG-mediated suppression of primary antibody responses in Fcgamma receptor-deficient mice
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1999 In: Proc Natl Acad Sci U S A, Vol. 96, no 5, p. 2244-2249Article in journal (Refereed) Published
Identifiers
urn:nbn:se:uu:diva-89553 (URN)
Available from: 2001-11-23 Created: 2001-11-23Bibliographically approved
2. IgE-mediated suppression of primary antibody responses in vivo
Open this publication in new window or tab >>IgE-mediated suppression of primary antibody responses in vivo
2001 In: Scand J Immunol, Vol. 53, p. 381-385Article in journal (Refereed) Published
Identifiers
urn:nbn:se:uu:diva-89554 (URN)
Available from: 2001-11-23 Created: 2001-11-23Bibliographically approved
3. IgG2a-mediated enhancement of antibody responses is dependent on FcRgamma+ bone marrow-derived cells
Open this publication in new window or tab >>IgG2a-mediated enhancement of antibody responses is dependent on FcRgamma+ bone marrow-derived cells
2001 In: Scand J Immunol, Vol. 54, p. 495-500Article in journal (Refereed) Published
Identifiers
urn:nbn:se:uu:diva-89555 (URN)
Available from: 2001-11-23 Created: 2001-11-23Bibliographically approved
4. IgG3 augments Ab responses in FcRgamma-deficient mice
Open this publication in new window or tab >>IgG3 augments Ab responses in FcRgamma-deficient mice
Manuscript (Other academic)
Identifiers
urn:nbn:se:uu:diva-89556 (URN)
Available from: 2001-11-23 Created: 2001-11-23 Last updated: 2010-01-13Bibliographically approved
5. FcgammaRIII-deficient mice are highly protected to collagen-induced arthritis
Open this publication in new window or tab >>FcgammaRIII-deficient mice are highly protected to collagen-induced arthritis
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Article in journal (Refereed) Submitted
Identifiers
urn:nbn:se:uu:diva-89557 (URN)
Available from: 2001-11-23 Created: 2001-11-23Bibliographically approved

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