%0 Journal Article
%T Fc¦Ã receptor targeting in RA
%A Toshiyuki Takai
%A Akira Nakamura
%A Akiko Tobinai
%A Shota Endo
%A Masanori Inui
%J Arthritis Research & Therapy
%D 2012
%I BioMed Central
%R 10.1186/ar3572
%X IgGFc receptors (Fc¦ÃRs) were originally identified as B cell surface molecules. For more than 40 years, Fc¦ÃRs 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 Fc¦ÃRs, which associate with homodimeric Fc receptor common ¦Ã subunits, are crucial for the onset and exacerbation of inflammatory diseases. In contrast, a unique inhibitory Fc¦ÃR, Fc¦ÃRIIB, 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 Fc¦ÃRs and the inhibitory Fc¦ÃRIIB in the initiation and suppression of inflammation, respectively [1-5].The ultimate goals of Fc¦ÃR 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 Fc¦ÃRs, recent studies have pointed out an indispensable role of Fc¦ÃRIIB 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 Fc¦ÃRs as potential therapeutic targets for various inflammatory diseases, along with the comparison withnon-Fc¦ÃR-mediated mechanisms of IVIg.
%U http://arthritis-research.com/content/14/S1/O17