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- Title
IgG3-Mediated Enhancement of the Antibody Response is Normal in FcγRI-Deficient Mice.
- Authors
Hjelm, F.; Carlsson, F.; Verbeek, S.; Heyman, B.
- Abstract
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 FcRγ–/– mice, reported to lack FcγRI and FcγRIII because of deletion of the common FcRγ chain. Also IgG3 can enhance antibody responses. However, this effect is unperturbed in FcRγ–/– mice but severely impaired in complement-depleted animals and in animals lacking complement receptor 1 and 2. Although this argues against involvement of FcγRs, FcRγ–/– mice may express one-fifth of the normal levels of FcγRI and, in addition, FcγRI has been suggested to bind IgG3. We re-investigated the dependence of IgG3-mediated enhancement on FcγRs using a mouse strain selectively lacking FcγRI 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 FcγRs in IgG3-mediated enhancement of antibody responses and support our previous conclusion that complement plays a major role.
- Subjects
IMMUNOGLOBULIN G; IMMUNOGLOBULINS; CELL proliferation; ANTIGENS; GENETICS; ERYTHROCYTES; MICE
- Publication
Scandinavian Journal of Immunology, 2005, Vol 62, Issue 5, p453
- ISSN
0300-9475
- Publication type
Article
- DOI
10.1111/j.1365-3083.2005.01684.x