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Role of FcγRI (CD64) in erythrocyte elimination and its up‐regulation in thalassaemia
Author(s) -
Edith Wiener,
DL Allen,
Richard W. Porter,
S. N. Wickramasinghe,
JB Porter,
Sriprapa Chinprasertsuk,
Uamporn Siripanyaphinyo,
Kovit Pattanapanyasat,
Suthat Fucharoen,
Wanchai Wanachiwanawin
Publication year - 1999
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.1999.01646.x
Subject(s) - cd64 , receptor , chemistry , stimulation , microbiology and biotechnology , immunology , medicine , endocrinology , biology
To examine any role of the high affinity Fcγ class I receptor (FcγRI) (CD64) in erythrocyte elimination by mononuclear phagocytes (MP) in thalassaemia (thal), we investigated the in vitro interaction of β‐thalassaemic erythrocytes with monocytes (Mo) whose FcγR expression had been modulated by cytokines. Treatment of Mo with interferon (IFN)‐γ or interleukin (IL)‐10 which up‐regulate FcγRI, caused a dose‐dependent increase in binding of β‐thalassaemic erythrocytes, whereas stimulation with IL‐4 which down‐regulates the receptor, reduced this interaction, in a dose‐dependent manner, to that of normal erythrocytes. Binding of thalassaemic erythrocytes by IFN‐γ or IL‐10‐treated Mo was inhibited by FcγRI‐specific reagents. In addition, Mo expression of FcγRI and HLA class II DR was determined by flow cytometry in Thai patients with HbH disease (α 1/ α 2 or α 1 /Hb Constant Spring) ( n = 15) or β°‐thal/HbE ( n = 16). In both groups of patients FcγRI expression was increased as compared to normal controls ( n = 14): mean fluorescence intensity (±SD) 124.79 ± 38.77 in HbH disease and 121.86 ± 18.23 in β°‐thal/HbE versus 91.94 ± 17.36 in normal controls ( P < 0.01 and P < 0.001, respectively). In contrast, HLA class II DR expression was similar in patients and controls. The results suggest that, in thalassaemia, up‐regulated FcγRI on mononuclear phagocytes plays a role in their interaction with erythrocytes and that this process can be modified by cytokines.