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肿瘤坏死因子-α通过CD11c/CD18分子诱导B淋巴细胞慢性淋巴细胞白血病细胞扩散。

TNF-alpha induces spreading of B-CLL via the CD11c/CD18 molecule.

作者信息

van Kooten C, Rensink I, Aarden L, van Oers R

机构信息

Central Laboratory, The Netherlands Red Cross Blood Transfusion Service, Amsterdam.

出版信息

Am J Hematol. 1993 Dec;44(4):221-8. doi: 10.1002/ajh.2830440402.

DOI:10.1002/ajh.2830440402
PMID:7901991
Abstract

Activation of malignant B cells can lead to extensive morphological changes of these cells. A combination of PMA and TNF-alpha can induce adherence of purified B-CLL cells, which acquire a dendritic cell-like appearance. This phenomenon that we have termed spreading, is accompanied by upregulation of expression of both beta 1 and beta 2 integrin molecules. Spreading was inhibited by the addition of antibodies against CD18 or CD11c. In other B cell malignancies (HCL and NHL), morphological changes could be induced by PMA in the absence of TNF-alpha. Culturing in the presence of prednisolone resulted in an inhibition of spreading, most likely mediated via a down regulation of CD18 and CD11c expression. These data indicate that the CD11c/CD18 complex might be important for the adhesive properties of B cells.

摘要

恶性B细胞的激活可导致这些细胞发生广泛的形态学变化。佛波酯(PMA)和肿瘤坏死因子-α(TNF-α)联合使用可诱导纯化的B细胞慢性淋巴细胞白血病(B-CLL)细胞黏附,这些细胞会呈现出树突状细胞样外观。我们将这种现象称为铺展,它伴随着β1和β2整合素分子表达的上调。添加抗CD18或CD11c抗体可抑制铺展。在其他B细胞恶性肿瘤(毛细胞白血病[HCL]和非霍奇金淋巴瘤[NHL])中,在没有TNF-α的情况下,PMA可诱导形态学变化。在泼尼松龙存在的情况下培养会导致铺展受到抑制,这很可能是通过下调CD18和CD11c表达介导的。这些数据表明,CD11c/CD18复合物可能对B细胞的黏附特性很重要。

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