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Intravenous immunoglobulin does not increase FcγRIIB expression levels on monocytes in children with immune thrombocytopenia
Author(s) -
Shimomura M.,
Hasegawa S.,
Seki Y.,
Fukano R.,
Hotta N.,
Ichiyama T.
Publication year - 2012
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.2012.04591.x
Subject(s) - cd14 , immunology , cd16 , antibody , fc receptor , monocyte , cd64 , peripheral blood mononuclear cell , medicine , immune system , immunoglobulin g , flow cytometry , platelet , immune thrombocytopenia , biology , in vitro , cd3 , biochemistry , cd8
Summary Intravenous immunoglobulin (IVIG) produces a rapid and prolonged increase in the platelet counts of children with immune thrombocytopenia (ITP). The mechanism of IVIG efficacy in a murine model of ITP has been reported to operate through an IVIG‐mediated increase in the expression of the inhibitory Fc receptor FcγRIIB(CD32B) on splenic macrophages. This investigation examined whether IVIG administration results in a similar increase in FcγRIIB expression on peripheral blood CD14 + monocytes in 20 children with ITP. FcγRIIB expression on peripheral blood monocytes was measured by flow cytometry in ITP patients, before and after IVIG therapy, as well as in control subjects. Peripheral blood monocytes were labelled with fluorescent‐specific antibodies. There were no significant differences in the percentages or numbers of CD14 + CD32B + monocytes, or in the percentage of CD14 + CD32B + monocytes present in children with ITP before and after IVIG therapy. We suggest that IVIG does not increase FcγRIIB expression in peripheral blood monocytes in children with ITP.

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