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通过与B淋巴细胞接触刺激人骨髓基质细胞酪氨酸激酶和白细胞介素-6的产生。

Stimulation of human bone marrow stromal cell tyrosine kinases and IL-6 production by contact with B lymphocytes.

作者信息

Jarvis L J, LeBien T W

机构信息

Department of Laboratory Medicine and Pathology, University of Minnesota Medical School, Minneapolis 55455, USA.

出版信息

J Immunol. 1995 Sep 1;155(5):2359-68.

PMID:7544372
Abstract

The interaction of normal human B cell precursors with the bone marrow (BM) stromal cells that support their growth and maturation is mediated by adhesion of B cell CD49d/CD29 (alpha 4 beta 1 integrin or VLA-4) to stromal cell signal transduction, we generated CD49d-deficient variants of the RAMOS early b Burkitt's lymphoma cell line. RAMOS was chosen due to its lack of expression of CD49e (alpha 5 integrin) and CD44, which could potentially interact with stromal cells or their extracellular matrix. In contrast to the parental RAMOS cell line, CD49d-deficient RAMOS cell lines did not adhere to primary human BM stromal cells. Tyrosine phosphorylation of several stromal cell proteins was stimulated within 5 to 10 min of contact with either CD49d-expressing or CD49d-deficient RAMOS. These proteins included a 110-kDa substrate tentatively identified as pp125FAK. In contrast, mAb cross-linking of stromal cell CD106 had no significant effect on protein tyrosine phosphorylation. Il-6 production by stromal cells was enhanced up to fourfold over 3 days when stromal cells were cultured in contact with RAMOS cells, regardless of CD49d expression. Stromal cell IL-6 production was not significantly enhanced by RAMOS cells cultured above the stromal cells in Transwell inserts. Thus, we have demonstrated through the use of paired CD49d-expressing and CD49d-deficient RAMOS cell lines that protein tyrosine kinase activity and IL-6 production by primary human BM stromal cells can be enhanced in a manner that is dependent on B cell contact but independent of CD49d-mediated adhesion. These results indicate the potential for B cells to interact with cells in their microenvironment and activate feedback mechanisms mediated by stromal cells, which may regulate lymphopoiesis.

摘要

正常人类B细胞前体与支持其生长和成熟的骨髓(BM)基质细胞之间的相互作用是由B细胞CD49d/CD29(α4β1整合素或VLA-4)与基质细胞信号转导的粘附介导的。我们构建了RAMOS早期B Burkitt淋巴瘤细胞系的CD49d缺陷变体。选择RAMOS是因为它不表达CD49e(α5整合素)和CD44,而这两种蛋白可能与基质细胞或其细胞外基质相互作用。与亲代RAMOS细胞系不同,CD49d缺陷的RAMOS细胞系不粘附于原代人BM基质细胞。与表达CD49d或CD49d缺陷的RAMOS接触5至10分钟内,几种基质细胞蛋白的酪氨酸磷酸化受到刺激。这些蛋白包括一种暂时鉴定为pp125FAK的110 kDa底物。相比之下,基质细胞CD106的单克隆抗体交联对蛋白酪氨酸磷酸化没有显著影响。当基质细胞与RAMOS细胞接触培养时,无论CD49d表达如何,基质细胞IL-6的产生在3天内可增强至四倍。在Transwell小室中,RAMOS细胞培养在基质细胞上方时,基质细胞IL-6的产生没有显著增强。因此,我们通过使用成对的表达CD49d和CD49d缺陷的RAMOS细胞系证明,原代人BM基质细胞的蛋白酪氨酸激酶活性和IL-6产生可以通过一种依赖于B细胞接触但独立于CD49d介导的粘附的方式增强。这些结果表明B细胞与微环境中的细胞相互作用并激活由基质细胞介导的反馈机制的潜力,这可能调节淋巴细胞生成。

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