SFA-1/PETA-3 (CD151), a member of the transmembrane 4 superfamily, associates preferentially with alpha 5 beta 1 integrin and regulates adhesion of human T cell leukemia virus type 1-infected T cells to fibronectin.

SFA-1/PETA-3 (CD151), a member of the transmembrane 4 superfamily, associates preferentially with alpha 5 beta 1 integrin and regulates adhesion of human T cell leukemia virus type 1-infected T cells to fibronectin.
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DOI:
10.4049/jimmunol.161.6.3087
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发表时间:
1998-09
影响因子:
4.4
通讯作者:
H. Hasegawa;Tetsuhiko Nomura;Kyoko Kishimoto;K. Yanagisawa;S. Fujita
H. Hasegawa;Tetsuhiko Nomura;Kyoko Kishimoto;K. Yanagisawa;S. Fujita
中科院分区:
医学2区
文献类型:
--
作者:
H. Hasegawa;Tetsuhiko Nomura;Kyoko Kishimoto;K. Yanagisawa;S. Fujita

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在这项研究中,我们分析了粘附分子相关的SFA-1/PETA-3(CD 151)的生物学功能,在人类T细胞白血病病毒1型(HTLV-1)感染的T细胞和新鲜分离的成人T细胞白血病(ATL)细胞使用抗CD 151单克隆抗体。抗CD 151 mAb从HTLV-1感染的T细胞共沉淀α 5 β 1整联蛋白。相反,抗α 5整联蛋白mAb共沉淀CD 151。抗CD 151 mAb抑制HTLV-1感染的T细胞与纤连蛋白的粘附,但对其与层粘连蛋白、I型胶原或IV型胶原的粘附没有任何影响。此外,反义CD 151寡核苷酸处理的HTLV-1感染的T细胞显示出对纤连蛋白粘附的显著抑制。这些发现表明,CD 151分子与α 5 β 1整联蛋白分子相关,并增强α 5 β 1整联蛋白介导的与纤连蛋白的粘附。此外,来自淋巴瘤型ATL患者淋巴结的ATL细胞上的CD 151、α 4 β 1整联蛋白和α 5 β 1整联蛋白的表达水平显著高于来自白血病型ATL患者的循环ATL细胞上的表达水平。这表明,这些整合素的表达增加可能有助于淋巴瘤的形成,通过ATL细胞的细胞外基质和树突状细胞的粘附,而不是有助于迁移。
In this study we have analyzed the adhesion molecules associated with and the biologic function of SFA-1/PETA-3 (CD151) in human T cell leukemia virus type 1 (HTLV-1)-infected T cells and in freshly isolated adult T cell leukemia (ATL) cells using an anti-CD151 mAb. The anti-CD151 mAb coprecipitated alpha 5 beta 1 integrin from HTLV-1-infected T cells. Conversely, an anti-alpha 5 integrin mAb coprecipitated CD151. The anti-CD151 mAb inhibited the adhesion of HTLV-1-infected T cells to fibronectin but did not have any effect on their adhesion to laminin, collagen type I, or collagen type IV. Moreover, antisense CD151 oligonucleotide-treated HTLV-1-infected T cells showed significant inhibition of adhesion to fibronectin. These findings showed that the CD151 molecule was associated with the alpha 5 beta 1 integrin molecule and that it enhanced alpha 5 beta 1 integrin-mediated adhesion to fibronectin. In addition, the expression levels of CD151, alpha 4 beta 1 integrin, and alpha 5 beta 1 integrin on ATL cells from lymph nodes of lymphoma-type ATL patients were significantly higher than those on circulating ATL cells from leukemia-type ATL patients. This suggests that the increased expression of these integrins may contribute to lymphoma formation through the adhesion of ATL cells to the extracellular matrix and dendritic cells, rather than contributing to transmigration.