TN/iNOS-producing dendritic cells mediate innate immune defense against bacterial infection

TN/iNOS-producing dendritic cells mediate innate immune defense against bacterial infection
复制标题

DOI:
10.1016/s1074-7613(03)00171-7
复制
发表时间:
2003-07-01
期刊:
影响因子:
32.4
通讯作者:
Pamer, EG
Pamer, EG
中科院分区:
医学1区
文献类型:
--
作者:
Serbina, NV;Salazar-Mather, TP;Pamer, EG

文献摘要

被引文献

相似文献

树突状细胞(dc)向T细胞提供微生物抗原,并提供调节T细胞分化的炎症信号。虽然dc在适应性免疫中的作用已经确立,但它们在先天免疫防御中的作用还不太明确。我们已经在单核细胞增生李斯特菌感染小鼠的脾脏中发现了一个TNF/ inos生成(Tip)-DC亚群,而在ccr2缺陷小鼠中则不存在。tip - dc的缺失导致严重的TNF和iNOS缺乏,无法清除原发性细菌感染。CD8和CD4 T细胞对单核增生乳杆菌抗原的反应在ccr2缺陷小鼠中得以保留,这表明tip - dc对T细胞启动不是必需的。在单核增生乳杆菌感染过程中,tip - dc作为TNF和iNOS的主要来源,协调和介导了针对这种细胞内细菌病原体的先天免疫防御。
Dendritic cells (DCs) present microbial antigens to T cells and provide inflammatory signals that modulate T cell differentiation. While the role of DCs in adaptive immunity is well established, their involvement in innate immune defenses is less well defined. We have identified a TNF/iNOS-producing (Tip)-DC subset in spleens of Listeria monocytogenes-infected mice that is absent from CCR2-deficient mice. The absence of Tip-DCs results in profound TNF and iNOS deficiencies and an inability to clear primary bacterial infection. CD8 and CD4 T cell responses to L. monocytogenes antigens are preserved in CCR2-deficient mice, indicating that Tip-DCs are not essential for T cell priming. Tip-DCs, as the predominant source of TNF and iNOS during L. monocytogenes infection, orchestrate and mediate innate immune defense against this intracellular bacterial pathogen.