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L3T4 + T细胞调节艾贝尔逊病毒诱导的淋巴瘤发生。

L3T4+ T cells regulate Abelson virus-induced lymphomagenesis.

作者信息

Infante A J, Boulware S, Cagle M

机构信息

Department of Pediatrics, University of Texas Health Science Center, San Antonio 78284.

出版信息

J Immunol. 1988 Apr 1;140(7):2462-5.

PMID:2965186
Abstract

To evaluate the role of T cells in regulation of lymphomagenesis, experiments were performed using Abelson murine leukemia virus (AMuLV). In vitro transformation of bone marrow target cells by this B lymphotropic retrovirus was inhibited by peripheral lymph node cells from naive mice. The inhibitory activity depended on Thy-1+ L3T4+ cells but did not require Lyt-2+ cells. In vivo depletion of L3T4+ T cells with a mAb (GK1.5) altered the course of AMuLV-induced lymphoma. L3T4 depletion of naturally resistant C57BL/6 mice resulted in dramatic susceptibility to lymphoma induction. Lymphoma cells from anti-L3T4-treated C57BL/6 mice infected with AMuLV displayed the B lineage transformation marker P1606C3. These studies reveal an important immunologic component of Abelson disease resistance involving L3T4+ T cells.

摘要

为评估T细胞在淋巴瘤发生调控中的作用,利用阿贝尔森鼠白血病病毒(AMuLV)开展了实验。这种嗜B淋巴细胞逆转录病毒对骨髓靶细胞的体外转化受到来自未接触过抗原的小鼠外周淋巴结细胞的抑制。抑制活性依赖于Thy-1⁺L3T4⁺细胞,但不需要Lyt-2⁺细胞。用单克隆抗体(GK1.5)在体内清除L3T4⁺T细胞改变了AMuLV诱导的淋巴瘤病程。用抗L3T4抗体清除天然抗性的C57BL/6小鼠的L3T4后,导致其对淋巴瘤诱导极度易感。感染AMuLV的经抗L3T4处理的C57BL/6小鼠的淋巴瘤细胞显示出B系转化标志物P1606C3。这些研究揭示了阿贝尔森病抗性中涉及L3T4⁺T细胞的重要免疫成分。

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