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Regulation of Antibody Responses via Antibodies, Complement, and Fc Receptors
Abstract
Antibodies can completely suppress or enhance the antibody response to their specific antigen by several hundredfold. Immunoglobulin M (IgM) enhances antibody responses via the complement system, and complement activation by IgM probably starts the chain of events leading to antibody responses to suboptimal antigen doses. IgG can enhance primary antibody responses in the absence of the complement system and seems to be dependent on Fc receptors for IgG (FcγRs). IgE enhances antibody responses via the low-affinity receptor for IgE (FcεRII/CD23). The precise effector mechanisms that cause enhancement are not known, but direct B-cell signaling, antigen presentation, and increased follicular localization are all possibilities. IgG, IgE, and IgM may also suppress antibody responses when used in certain immunization regimes, and it seems reasonable that an important mechanism behind suppression is the masking of antigenic epitopes by antibodies. In addition, FcγRIIB, which contains a cytoplasmic inhibitory motif, acts as a negative regulator of antibody responses. This receptor, however, may prevent the antibody responses from exceeding a certain level rather than causing complete suppression.
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Cites
Wessels, M. R., Butko, P., Ma, M., Warren, H. B., Lage, A. L., & Carroll, M. C. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.25.11490 · Cited by 503
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Fecteau, J. F., Côté, G., & Néron, S. (2006) · The Journal of Immunology · doi:10.4049/jimmunol.177.6.3728 · Cited by 298
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Metadata
- Authors
- Heyman, B.
- Venue
- Annual Review of Immunology
- Publisher
- Annual Reviews
- Published
- 2000-04
- Volume
- 18
- Issue
- 1
- Pages
- 709-737
- ISSN
- 0732-0582 (ISSN-L)
- 1545-3278
- OpenAlex
- W2112676752
- Cited by
- 353
- References
- 1
- FWCI
- 3.89
- Type
- journal article
- Language
- en
- Open access
- closed
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- Heyman, B. (2000). Regulation of Antibody Responses via Antibodies, Complement, and Fc Receptors. Annual Review of Immunology. https://doi.org/10.1146/annurev.immunol.18.1.709
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
