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细胞因子调节单核细胞系细胞及类风湿性关节炎滑膜中活化白细胞细胞黏附分子(CD166)的表达。

Cytokine-regulated expression of activated leukocyte cell adhesion molecule (CD166) on monocyte-lineage cells and in rheumatoid arthritis synovium.

作者信息

Levesque M C, Heinly C S, Whichard L P, Patel D D

机构信息

Duke University Medical Center, Durham, North Carolina 27710, USA.

出版信息

Arthritis Rheum. 1998 Dec;41(12):2221-9. doi: 10.1002/1529-0131(199812)41:12<2221::AID-ART18>3.0.CO;2-I.

DOI:10.1002/1529-0131(199812)41:12<2221::AID-ART18>3.0.CO;2-I
PMID:9870879
Abstract

OBJECTIVE

To determine whether monocyte/macrophage expression of the CD6 ligand, activated leukocyte cell adhesion molecule (ALCAM) (CD166), is regulated by cytokines during inflammation in rheumatoid arthritis (RA).

METHODS

We used flow cytometry to test whether cytokines present in rheumatoid synovium could regulate ALCAM cell surface expression on peripheral blood (PB) monocytes and RA synovial fluid (SF) macrophages, and we examined ALCAM expression in situ in RA synovium by immunofluorescence.

RESULTS

The monocyte differentiation factors interleukin-3, macrophage colony-stimulating factor (M-CSF), and granulocyte-macrophage colony-stimulating factor augmented ALCAM expression on PB monocytes. ALCAM was expressed on monocyte-lineage cells in situ in inflamed synovium from patients with RA (9 of 9), but not in uninflamed synovium from patients with joint trauma (0 of 3). Furthermore, in vitro culture-induced ALCAM expression on PB monocytes and CD14+ RA SF cells was inhibited by an M-CSF neutralizing antibody.

CONCLUSION

ALCAM expression on PB and SF monocytes/macrophages is enhanced by M-CSF.

摘要

目的

确定类风湿关节炎(RA)炎症过程中,单核细胞/巨噬细胞上CD6配体即活化白细胞黏附分子(ALCAM,CD166)的表达是否受细胞因子调控。

方法

我们采用流式细胞术检测类风湿滑膜中存在的细胞因子是否能调节外周血(PB)单核细胞和RA滑膜液(SF)巨噬细胞上ALCAM的细胞表面表达,并通过免疫荧光检查RA滑膜中ALCAM的原位表达。

结果

单核细胞分化因子白细胞介素-3、巨噬细胞集落刺激因子(M-CSF)和粒细胞-巨噬细胞集落刺激因子可增强PB单核细胞上ALCAM的表达。ALCAM在RA患者炎症滑膜的单核细胞系细胞上原位表达(9例中的9例),但在关节创伤患者的非炎症滑膜中不表达(3例中的0例)。此外,M-CSF中和抗体可抑制体外培养诱导的PB单核细胞和CD14⁺ RA SF细胞上ALCAM的表达。

结论

M-CSF可增强PB和SF单核细胞/巨噬细胞上ALCAM的表达。

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