Preexposure to live Brugia malayi microfilariae alters the innate response of human dendritic cells to Mycobacterium tuberculosis.
Preexposure to live Brugia malayi microfilariae alters the innate response of human dendritic cells to Mycobacterium tuberculosis.
复制标题
预先暴露于活的马来丝虫微丝蚴会改变人类树突状细胞对结核分枝杆菌的先天反应。
DOI：
10.1086/498912
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发表时间：
2006
期刊：
影响因子：
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通讯作者：
Nutman,ThomasB
中科院分区：
文献类型：
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作者：
Talaat,KawsarR;Bonawitz,RachaelE;Domenech,Pilar;Nutman,ThomasB
背景结核分枝杆菌和蠕虫的混合感染非常普遍，蠕虫的存在可能调节Th1反应的必要形式。方法体外分离人单核细胞，分化为树突状细胞(DC)和巨噬细胞，暴露于活的微丝虫(MF)中。MF对M的影响。结果与未暴露的结核分枝杆菌感染细胞相比，感染结核分枝杆菌的巨噬细胞CD14、CD54和人类白细胞抗原DR的表达降低，而感染结核分枝杆菌的巨噬细胞CD40的表达减少。暴露于MF的DC和M。感染结核病的DC比未暴露的结核分枝杆菌感染的树突状细胞产生更多的白介素1β。此外，暴露于MF的、感染结核分枝杆菌的DC和巨噬细胞比未暴露的结核分支杆菌感染的细胞表达更少的IL-10和干扰素-α。当它们与自体CD+T细胞培养时，暴露于MF的、感染结核分枝杆菌的DC比其他DC刺激干扰素-γ的能力更弱。树突状细胞暴露于MF后，DC特异性细胞间黏附分子-3结合非整合素的表面表达减少，而非整合素是M所需的受体。结核进入DC的可能性结论暴露于MF会减少DC表面的一个关键受体，这可能使这些细胞不太容易感染M。肺结核。暴露于MF会改变DC和巨噬细胞表面黏附和共刺激分子的表达，并改变它们的细胞因子和趋化因子的表达，从而降低它们的免疫反应能力
BackgroundMycobacterium tuberculosisand helminth coinfection is highly prevalent, and the presence of helminths may modulate the Th1 response necessary forM. tuberculosiscontrolMethodsElutriated human monocytes, differentiated into dendritic cells (DCs) and macrophages, were exposed in vitro to live microfilariae (mf). The influence that mf had onM. tuberculosisinfectivity, expression of cell surface molecules, and production of cytokines was determinedResultsCompared with mf-unexposed,M. tuberculosis–infected cells, mf-exposed,M. tuberculosis–infected DCs had decreased expression of CD14, CD54, and human leukocyte antigen–DR, and mf-exposed,M. tuberculosis–infected macrophages had decreased expression of CD40. DCs that were mf exposed andM. tuberculosisinfected produced more interleukin (IL)–1β than did mf-unexposed,M. tuberculosis–infected DCs. Also, mf-exposed,M. tuberculosis–infected DCs and macrophages expressed less IL-10 and interferon (IFN)–α than did mf-unexposed,M. tuberculosis–infected cells. When they were cultured with autologous CD4+T cells, mf-exposed,M. tuberculosis–infected DCs were less capable of stimulating the production of IFN-γ than were other DCs. Exposure of DCs to mf decreased the surface expression of DC–specific intercellular adhesion molecule–3 grabbing nonintegrin, a receptor required byM. tuberculosisfor entry into DCsConclusionsExposure to mf reduces a key receptor on the DC surface, which perhaps renders these cells less susceptible to infection withM. tuberculosis. Exposure to mf changes the surface expression of adhesion and costimulatory molecules on DCs and macrophages and alters their expression of cytokines and chemokines in a way that renders them less capable of immunologic responses