细胞因子对滑膜B型细胞上黏附分子的诱导作用。
Cytokine induction of adhesion molecules on synovial type B cells.
作者信息
Cicuttini F M, Martin M, Boyd A W
机构信息
Lions Clinical Cancer Research Laboratory, Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Australia.
出版信息
J Rheumatol. 1994 Mar;21(3):406-12.
OBJECTIVES
To study the role of cytokines on adhesion molecule expression and binding of activated T cells to synovial type B cells.
METHODS
Adhesion molecule expression was examined by immunofluorescence and adhesion of 51Cr-labelled T cells to the synovial cells determined.
RESULTS
Tumor necrosis factor alpha/interferon gamma (TNF alpha/IFN-gamma) and interleukin 1 alpha (IL-1 alpha)/IFN-gamma enhanced adhesion molecule expression and the adhesion of T cells to synovial cells. Anti-intercellular adhesion molecule 1 blocked adhesion of T cells to TNF alpha/IFN-gamma and IL-1 alpha/IFN-gamma stimulated synovial cells while an antibody to CD61 blocked adhesion to IL-1 alpha/IFN-gamma stimulated cells.
CONCLUSIONS
The interaction of leukocytes with adhesion molecules on synovial cells may play a role in recruitment of these cells to an inflammatory site.
目的
研究细胞因子对活化T细胞黏附分子表达及与滑膜B型细胞结合的作用。
方法
采用免疫荧光法检测黏附分子表达，并测定51Cr标记的T细胞与滑膜细胞的黏附情况。
结果
肿瘤坏死因子α/干扰素γ（TNFα/IFN-γ）和白细胞介素1α（IL-1α）/IFN-γ增强了黏附分子表达及T细胞与滑膜细胞的黏附。抗细胞间黏附分子1可阻断T细胞与TNFα/IFN-γ及IL-1α/IFN-γ刺激的滑膜细胞的黏附，而抗CD61抗体可阻断T细胞与IL-1α/IFN-γ刺激细胞的黏附。
结论
白细胞与滑膜细胞上黏附分子的相互作用可能在这些细胞募集至炎症部位的过程中发挥作用。
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