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白细胞介素4和13上调人结肠上皮细胞系中cd44的表达。

Interleukins 4 and 13 upregulate expression of cd44 in human colonic epithelial cell lines.

作者信息

Trejdosiewicz L K, Morton R, Yang Y, Banks R E, Selby P J, Southgate J

机构信息

ICRF Cancer Medicine Research Unit, St James's University Hospital, Leeds, LS9 7TF, UK.

出版信息

Cytokine. 1998 Oct;10(10):756-65. doi: 10.1006/cyto.1998.0361.

DOI:10.1006/cyto.1998.0361
PMID:9811528
Abstract

Interleukin 4 (IL-4) inhibits carcinoma cell growth and promotes expression of differentiation-associated products by normal and malignant epithelial cells. The effects of IL-4 and IL-13 on expression of the CD44 transmembrane adhesion receptor were examined in human epithelial cell lines of colonic (HT-29, CaCo-2, DLD-1, T84), breast (MCF-7, ZR75-1) and liver (Hep-G2, PLC/PRF/5) origins as well as mitogen-activated and resting peripheral blood lymphocytes (PBL) and T cell lines (Jurkat, HUT78). Liver and Jurkat cells were negative for CD44. Colonic, breast and HUT78 cells expressed CD44 constitutively and all except DLD-1 and HUT78 also expressed CD44 splice variant (CD44v) epitopes. All cell lines expressed IL-4 receptors, but IL-4 and IL-13 induced upregulation of CD44 only in the colonic cell lines. CD44v was also upregulated, but there was no de novo induction of CD44v in variant-negative cells and no de novo expression of CD44 in the CD44(-) lines. CD44 upregulation in mitogen-activated PBL was not increased by IL-4 and IL-13 and was not inhibited by neutralizing antibodies. Other cytokines tested [interferon gamma (IFN-gamma, tumour necrosis factor alpha (TNF-alpha), transforming growth factor beta1 (TGF-beta1) and IL-6] did not affect CD44 core epitope expression in the cell lines tested.

摘要

白细胞介素4(IL-4)可抑制癌细胞生长,并促进正常和恶性上皮细胞表达分化相关产物。我们检测了IL-4和IL-13对结肠(HT-29、CaCo-2、DLD-1、T84)、乳腺(MCF-7、ZR75-1)和肝脏(Hep-G2、PLC/PRF/5)来源的人上皮细胞系以及丝裂原激活的和静息的外周血淋巴细胞(PBL)和T细胞系(Jurkat、HUT78)中CD44跨膜黏附受体表达的影响。肝脏细胞和Jurkat细胞的CD44呈阴性。结肠、乳腺和HUT78细胞组成性表达CD44,除DLD-1和HUT78外,其他细胞也表达CD44剪接变体(CD44v)表位。所有细胞系均表达IL-4受体,但IL-4和IL-13仅在结肠细胞系中诱导CD44上调。CD44v也上调,但在变体阴性细胞中未出现CD44v的从头诱导,在CD44(-)细胞系中也未出现CD44的从头表达。IL-4和IL-13未增加丝裂原激活的PBL中CD44的上调,且不受中和抗体的抑制。所检测的其他细胞因子[干扰素γ(IFN-γ)、肿瘤坏死因子α(TNF-α)、转化生长因子β1(TGF-β1)和IL-6]均未影响所检测细胞系中CD44核心表位的表达。

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