...
首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >IFN-gamma and IL-12 differentially regulate CC-chemokine secretion and CCR5 expression in human T lymphocytes.
【24h】

IFN-gamma and IL-12 differentially regulate CC-chemokine secretion and CCR5 expression in human T lymphocytes.

机译:IFN-γ和IL-12差异性调节人T淋巴细胞中CC趋化因子的分泌和CCR5表达。

获取原文
获取原文并翻译 | 示例
           

摘要

Interleukin (IL)-12, especially in the presence of neutralizing anti-IL-4 monoclonal antibodies, primed CD45RO(-) T clones for high CCL3/macrophage-inflammatory protein-1alpha (MIP-1alpha) and CCL4/MIP-1beta levels. In CD4(+) and CD8(+) clones from two patients deficient for IL-12Rbeta1 (IL-12Rbeta1(-/-)), production of CCL3/MIP-1alpha and CCL4/MIP-1beta was defective. CD4(+) clones from two patients deficient for interferon-gamma (IFN-gamma) R1 (IFN-gammaR1(-/-)) produced somewhat decreased CCL4/MIP-1beta levels. IL-12 failed to prime CD4(+) or CD8(+) healthy clones for high CCL5/regulated on activation, normal T expressed and secreted (RANTES) production, although its secretion was impaired in CD4(+) clones from IL-12Rbeta1(-/-) and IFN-gammaR1(-/-) patients. CCR5 surface expression was up-regulated in resting peripheral blood mononuclear cells and CD4(+) clones from both kinds of patients, rendering them more susceptible to CCR5-dependent (R5) HIV-1 infection. Neutralization of IFN-gamma increased CCR5 expression and decreased CC-chemokine secretion by CD4(+) clones from healthy and IL-12Rbeta1(-/-) individuals, suggesting an IFN-gamma-dependent control of CCR5 expression. These data provide the first documented analysis of chemokine secretion and chemokine receptor expression on T cells from IL-12 and IFN-gamma receptor-deficient patients and dissect the role of IL-12 and IFN-gamma on inducing inflammatory chemokine secretion and down-regulating CCR5 expression in human T cells.
机译:白介素(IL)-12,特别是在存在中和性抗IL-4单克隆抗体的情况下,引发了高CCL3 /巨噬细胞炎性蛋白-1alpha(MIP-1alpha)和CCL4 / MIP-1beta水平的CD45RO(-)T克隆。在来自两个缺乏IL-12Rbeta1(IL-12Rbeta1(-/-))的患者的CD4(+)和CD8(+)克隆中,CCL3 / MIP-1alpha和CCL4 / MIP-1beta的产生是有缺陷的。来自缺乏干扰素-γ(IFN-γ)R1(IFN-gammaR1(-/-))的两名患者的CD4(+)克隆产生的CCL4 / MIP-1beta水平有所降低。 IL-12无法启动CD4(+)或CD8(+)健康克隆以获得较高的CCL5 /在激活,正常T表达和分泌(RANTES)生产时受到调节,尽管其分泌在IL-12Rbeta1的CD4(+)克隆中受到了损害。 (-/-)和IFN-gammaR1(-/-)患者。在两种患者的静息外周血单核细胞和CD4(+)克隆中,CCR5表面表达均上调,使它们更容易受到CCR5依赖性(R5)HIV-1感染。 IFN-γ的中和增加了CCR5表达,并减少了来自健康和IL-12Rbeta1(-/-)个人的CD4(+)克隆的CD4(+)克隆的CC趋化因子分泌,表明CCR5表达受IFN-γ依赖性控制。这些数据为IL-12和IFN-γ受体缺陷患者的T细胞上的趋化因子分泌和趋化因子受体表达提供了首次文献记录的分析,并剖析了IL-12和IFN-γ在诱导炎症性趋化因子分泌和下调中的作用。 CCR5在人T细胞中的表达。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号