Expression of FC∈II/CD23 on Human Neutrophils Isolated from Rheumatoid Arthritis Patients

被引:0
|
作者
Antonio Vella
Paolo Bellavite
Alessandra Adami
Riccardo Ortolani
Giuseppina Benoni
Antonio Carletto
Domenico Biasi
Paola Caramaschi
Giuseppe Tridente
机构
[1] Institute of Immunology and Infectious Diseases,Institute of Pharmacology
[2] University of Verona,Department of Clinical and Experimental Medicine
[3] University of Verona,Clinical Chemistry and Microscopy
[4] University of Verona,undefined
来源
Inflammation | 1999年 / 23卷
关键词
Rheumatoid Arthritis; Control Subject; Adhesion Molecule; Rheumatoid Arthritis Patient; Inflammatory Disease;
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学科分类号
摘要
CD23, the low affinity receptor for IgE, is a 45 kilodalton molecule belonging to the C-type lectin family, some members of which have been identified as adhesion molecules. Since it has been described upregulated in different cells in chronic inflammatory diseases and in rheumatoid arthritis in particular, where neutrophils are directly involved in tissue damage, our interest, in this work, has been focused on the expression and regulation of this antigen on neutrophil membrane. We studied 22 patients suffering from rheumatoid arthritis and 22 healthy control subjects. CD23 expression on neutrophil membrane was analyzed by immunofluorescence. Neutrophils of 9 out of 22 patients expressed CD23 molecules, neutrophils of 11 out of 22 patients expressed CD23 only after 24 h of incubation in RPMI; only 2 out of 22 patients did not express the CD23 antigen on neutrophil membrane either after isolation or after a 24 h incubation. On the contrary neutrophils isolated from healthy subjects did not express CD23 molecules upon isolation. Only in 7/22 control subjects neutrophils resulted positive after 24 h of incubation in RPMI. Moreover, we found that in our experimental conditions the presence of IFN-g or GM-CSF alone or in combination with IL-4 inhibited CD23 expression during the 24 h incubation. Our results show that there is a strong association between neutrophil ability to express CD23 and rheumatoid arthritis, and that such expression may be regulated by GM-CSF, IFN-γ and IL-4.
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页码:471 / 479
页数:8
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