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Cited by 543

The DOI matches its Crossref record; 141 of the 141 references it cites were found in a registry or an index.

FcγRIIB in autoimmunity and infection: evolutionary and therapeutic implications

Open access
Smith, Kenneth G. C., Clatworthy, Menna R.·2010·Nature Reviews Immunology

Abstract

FcγRIIB is the only inhibitory Fc receptor. It controls many aspects of immune and inflammatory responses, and variation in the gene encoding this protein has long been associated with susceptibility to autoimmune disease, particularly systemic lupus erythematosus (SLE). FcγRIIB is also involved in the complex regulation of defence against infection. A loss-of-function polymorphism in FcγRIIB protects against severe malaria, the investigation of which is beginning to clarify the evolutionary pressures that drive ethnic variation in autoimmunity. Our increased understanding of the function of FcγRIIB also has potentially far-reaching therapeutic implications, being involved in the mechanism of action of intravenous immunoglobulin, controlling the efficacy of monoclonal antibody therapy and providing a direct therapeutic target.

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Metadata

Authors
Smith, K. G. C., & Clatworthy, M. R.
Venue
Nature Reviews Immunology
Published
2010-05
Volume
10
Issue
5
Pages
328-343
ISSN
  • 1474-1733 (ISSN-L)
  • 1474-1741
OpenAlex
W2088002019
Cited by
543
References
141
FWCI
3.68
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: FcγRIIB in autoimmunity and infection: evolutionary and therapeutic implications. https://app.cochat.ai/papers/10.1038/nri2762
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Smith, K. G. C., & Clatworthy, M. R. (2010). FcγRIIB in autoimmunity and infection: evolutionary and therapeutic implications. Nature Reviews Immunology. https://doi.org/10.1038/nri2762

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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.