Fcγ receptor expression on splenic macrophages in adult immune thrombocytopeniaстатья из журнала
Аннотация: Splenic macrophages play a key role in immune thrombocytopenia (ITP) pathogenesis by clearing opsonized platelets. Fcγ receptors (FcγR) participate in this phenomenon, but their expression on splenic macrophages and their modulation by treatment have scarcely been studied in human ITP. We aimed to compare the phenotype and function of splenic macrophages between six controls and 24 ITP patients and between ITP patients according to the treatments they received prior to splenectomy. CD86, human leucocyte antigen D-related (HLA-DR) and FcγR expression were measured by flow cytometry on splenic macrophages. The major FcγR polymorphisms were determined and splenic macrophage function was assessed by a phagocytosis assay. The expression of the activation markers CD86 and HLA-DR was higher on splenic macrophages during ITP compared to controls. While the expression of FcγR was not different between ITP and controls, the phagocytic function of splenic macrophages was reduced in ITP patients treated with intravenous immunoglobulin (IVIg) within the 2 weeks prior to splenectomy. The FCGR3A (158V/F) polymorphism, known to increase the affinity of FcγRIII to IgG, was over-represented in ITP patients. Thus, these are the first results arguing for the fact that the therapeutic use of IVIg during human chronic ITP does not modulate FcγR expression on splenic macrophages but decreases their phagocytic capabilities.
Год издания: 2017
Авторы: S. Audia, Kim Santegoets, G. Laarhoven, Gestur Vidarsson, Olivier Facy, Pablo Ortega‐Deballon, M. Samson, Nona Janikashvili, Philippe Saas, Bernard Bonnotte, TRDJ Radstake
Издательство: Oxford University Press
Источник: Clinical & Experimental Immunology
Ключевые слова: Platelet Disorders and Treatments, Monoclonal and Polyclonal Antibodies Research, Autoimmune Bullous Skin Diseases
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PubMed Central (HTML)
PubMed (HTML)
Clinical & Experimental Immunology (HTML)
HAL (Le Centre pour la Communication Scientifique Directe) (HTML)
HAL (Le Centre pour la Communication Scientifique Directe) (HTML)
PubMed Central (HTML)
PubMed (HTML)
Открытый доступ: bronze
Том: 188
Выпуск: 2
Страницы: 275–282