美國(guó)斯坦福大學(xué)醫(yī)學(xué)院Shirit Einav等研究人員合作通過(guò)系統(tǒng)免疫學(xué)方法確定嚴(yán)重登革熱進(jìn)展的全局和細(xì)胞類型特異性免疫特征。相關(guān)論文于2023年10月23日在線發(fā)表在《自然—免疫學(xué)》雜志上。
為了確定兒童血液中登革病毒（DENV）的靶細(xì)胞和嚴(yán)重登革熱（SD）進(jìn)展的免疫學(xué)特征，研究人員整合了兩種捕獲細(xì)胞和病毒元件的單細(xì)胞方法：包含病毒的單細(xì)胞RNA測(cè)序（viscRNA-Seq 2）和帶有分泌組分析和功能測(cè)試的靶向蛋白質(zhì)組學(xué)。除了髓系細(xì)胞外，在自然感染中，B細(xì)胞也蘊(yùn)藏著能感染許可細(xì)胞的復(fù)制DENV。細(xì)胞類型豐度、基因和蛋白質(zhì)表達(dá)與分泌以及細(xì)胞間通訊的改變表明，SD進(jìn)展者的免疫細(xì)胞遷移和炎癥反應(yīng)加劇。
同時(shí)，SD進(jìn)展者的抗原遞呈細(xì)胞顯示出完整的攝取，但干擾素反應(yīng)和抗原處理及遞呈特征受損，這些特征部分受DENV調(diào)節(jié)。SD進(jìn)展者的特征還包括效應(yīng)反應(yīng)的激活、調(diào)節(jié)和耗竭增加，以及HLA-DR表達(dá)的適應(yīng)性類NK細(xì)胞的擴(kuò)增。這些發(fā)現(xiàn)揭示了人體血液中的DENV靶細(xì)胞，并提供了對(duì)抗體介導(dǎo)的增強(qiáng)之外的SD發(fā)病機(jī)制見(jiàn)解。
據(jù)了解，SD是發(fā)病和死亡的主要原因。
附：英文原文
Title: Global and cell type-specific immunological hallmarks of severe dengue progression identified via a systems immunology approach
Author: Ghita, Luca, Yao, Zhiyuan, Xie, Yike, Duran, Veronica, Cagirici, Halise Busra, Samir, Jerome, Osman, Ilham, Rebelln-Snchez, David Esteban, Agudelo-Rojas, Olga Lucia, Sanz, Ana Maria, Sahoo, Malaya Kumar, Robinson, Makeda L., Gelvez-Ramirez, Rosa Margarita, Bueno, Nathalia, Luciani, Fabio, Pinsky, Benjamin A., Montoya, Jose G., Estupian-Cardenas, Maria Isabel, Villar-Centeno, Luis Angel, Rojas-Garrido, Elsa Marina, Rosso, Fernando, Quake, Stephen R., Zanini, Fabio, Einav, Shirit
Issue&Volume: 2023-10-23
Abstract: Severe dengue (SD) is a major cause of morbidity and mortality. To define dengue virus (DENV) target cells and immunological hallmarks of SD progression in children’s blood, we integrated two single-cell approaches capturing cellular and viral elements: virus-inclusive single-cell RNA sequencing (viscRNA-Seq 2) and targeted proteomics with secretome analysis and functional assays. Beyond myeloid cells, in natural infection, B cells harbor replicating DENV capable of infecting permissive cells. Alterations in cell type abundance, gene and protein expression and secretion as well as cell–cell communications point towards increased immune cell migration and inflammation in SD progressors. Concurrently, antigen-presenting cells from SD progressors demonstrate intact uptake yet impaired interferon response and antigen processing and presentation signatures, which are partly modulated by DENV. Increased activation, regulation and exhaustion of effector responses and expansion of HLA-DR-expressing adaptive-like NK cells also characterize SD progressors. These findings reveal DENV target cells in human blood and provide insight into SD pathogenesis beyond antibody-mediated enhancement.
來(lái)源：科學(xué)網(wǎng)
原標(biāo)題：科學(xué)家確定嚴(yán)重登革熱進(jìn)展的全局和細(xì)胞類型特異性免疫特征
作者：小柯
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