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This article is part of the supplement: Proceedings of the 8th Global Arthritis Research Network (GARN) Meeting and 1st Bio-Rheumatology International Congress (BRIC)

Oral presentation

Fcγ receptor targeting in RA

Toshiyuki Takai1*, Akira Nakamura12, Akiko Tobinai1, Shota Endo1 and Masanori Inui1

  • * Corresponding author: Toshiyuki Takai

Author affiliations

1 Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan

2 Department of Immunology, Kanazawa Medical University, Ishikawa 920-0293, Japan

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Citation and License

Arthritis Research & Therapy 2012, 14(Suppl 1):O17  doi:10.1186/ar3572


The electronic version of this article is the complete one and can be found online at: http://arthritis-research.com/content/14/S1/O17


Published:9 February 2012

© 2012 Takai et al.; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Oral presentation

The activation threshold of cells in the immune system is often tuned by cell surface molecules. Among these, Fc receptors expressed on various hematopoietic cells constitute critical elements for activating or down-modulating immune responses.

IgGFc receptors (FcγRs) were originally identified as B cell surface molecules. For more than 40 years, FcγRs have continued to attract the interest of many basic researchers and clinicians due to their intriguing IgG binding ability, which provides a critical link between the humoral and cellular branches of the immune system.

Several activating-type FcγRs, which associate with homodimeric Fc receptor common γ subunits, are crucial for the onset and exacerbation of inflammatory diseases. In contrast, a unique inhibitory FcγR, FcγRIIB, plays a critical role in keeping immune cells silent. Murine models for allergic responses and autoimmune diseases including RA illustrate the indispensable roles of activating-type FcγRs and the inhibitory FcγRIIB in the initiation and suppression of inflammation, respectively [1-5].

The ultimate goals of FcγR research are to accomplish our understanding of this molecular family and to delineate novel therapeutic strategies toward the conquest of allergic and autoimmune diseases, infectious diseases, immunodeficiency, transplantation-associated immune disorders, and malignant tumors. Although many lines of evidence indicate that a part of the intravenous Ig (IVIg)-mediated anti-inflammatory effects can be attributable to the blocking of activating-type FcγRs, recent studies have pointed out an indispensable role of FcγRIIB in therapeutic benefits of IVIg in several murine models of inflammatory diseases including RA [6]. In this session, we will give a brief summary of recent knowledge on antibody biomedicine including IVIgto you, in light of exploiting FcγRs as potential therapeutic targets for various inflammatory diseases, along with the comparison withnon-FcγR-mediated mechanisms of IVIg.

References

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  5. Takai T, Ono M, Hikida M, Ohmori H, Ravetch JV: Augmented humoral and anaphylactic responses in FcγRII-deficient mice.

    Nature 1996, 379:346-349. PubMed Abstract | Publisher Full Text OpenURL

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