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As these antibodies may be a potential replacement for intravenous immune globulin (<jats:styled-content style=\"fixed-case\">IVIG<\/jats:styled-content>) in the treatment of <jats:styled-content style=\"fixed-case\">ITP<\/jats:styled-content> and other autoimmune diseases, an understanding of their mechanisms of action is important. The role of the inhibitory <jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>c receptor (<jats:styled-content style=\"fixed-case\">Fc\u03b3RIIb<\/jats:styled-content>) in the mechanism of action of <jats:styled-content style=\"fixed-case\">IVIG<\/jats:styled-content> and therapeutic <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>44 antibodies remains uncertain. To assess if <jats:styled-content style=\"fixed-case\">Fc\u03b3RIIb<\/jats:styled-content> in splenic macrophages plays a critical role in the action of these two therapeutics, splenectomized mice and mice genetically deficient in <jats:styled-content style=\"fixed-case\">Fc\u03b3RIIb<\/jats:styled-content> on different backgrounds were evaluated.<\/jats:p><\/jats:sec><jats:sec><jats:title>Study Design and Methods<\/jats:title><jats:p>Thrombocytopenia was induced in <jats:styled-content style=\"fixed-case\">Fc\u03b3RIIb<\/jats:styled-content>\u2010deficient mice on <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>6;129<jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>, <jats:styled-content style=\"fixed-case\">C57BL<\/jats:styled-content>\/6, and <jats:styled-content style=\"fixed-case\">BALB<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">C<\/jats:styled-content> backgrounds, as well as splenectomized mice and control mice by platelet (<jats:styled-content style=\"fixed-case\">PLT<\/jats:styled-content>) antibody. <jats:styled-content style=\"fixed-case\">PLT<\/jats:styled-content> counts were enumerated before and after treatment with anti\u2010<jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>44, red blood cell antibodies, or <jats:styled-content style=\"fixed-case\">IVIG<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Anti\u2010<jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>44 is ineffective at inhibiting thrombocytopenia in <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>6;129<jats:styled-content style=\"fixed-case\">S Fc\u03b3RIIb<\/jats:styled-content>\u2010deficient mice but, like <jats:styled-content style=\"fixed-case\">IVIG<\/jats:styled-content>, is effective in splenectomized mice and <jats:styled-content style=\"fixed-case\">Fc\u03b3RIIb<\/jats:styled-content>\u2010deficient mice on the <jats:styled-content style=\"fixed-case\">BALB<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">C<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">C57BL<\/jats:styled-content>\/6 background.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>These data suggest that 1) the <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>6;129<jats:styled-content style=\"fixed-case\">S<\/jats:styled-content> background itself is unlikely to be the sole reason for anti\u2010<jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>44's inability to function in <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>6;129<jats:styled-content style=\"fixed-case\">S Fc\u03b3RIIb<\/jats:styled-content>\u2010deficient mice, 2) the simple loss of macrophage <jats:styled-content style=\"fixed-case\">Fc\u03b3RIIb<\/jats:styled-content> expression alone is insufficient to explain anti\u2010<jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>44 ameliorative function, and 3) a combination of mouse background genes in addition to <jats:styled-content style=\"fixed-case\">Fc\u03b3RIIb<\/jats:styled-content> genetic disruption may affect the ability of anti\u2010<jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>44 to function therapeutically. Similarities between <jats:styled-content style=\"fixed-case\">IVIG<\/jats:styled-content> and anti\u2010<jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>44 mechanisms suggest that patients responsive to <jats:styled-content style=\"fixed-case\">IVIG<\/jats:styled-content> may also potentially respond to anti\u2010<jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>44 treatment.<\/jats:p><\/jats:sec>","DOI":"10.1111\/trf.12957","type":"journal-article","created":{"date-parts":[[2014,12,15]],"date-time":"2014-12-15T07:44:45Z","timestamp":1418629485000},"page":"1492-1500","source":"Crossref","is-referenced-by-count":12,"title":["<scp>CD<\/scp>44 antibody\u2013mediated amelioration of murine immune thrombocytopenia (ITP): mouse background determines the effect of <scp>Fc<\/scp>\u03b3RIIb genetic disruption"],"prefix":"10.1111","volume":"55","author":[{"given":"Andrew R.","family":"Crow","sequence":"first","affiliation":[{"name":"Canadian Blood Services 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