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疟疾诱导的干扰素-γ驱动Tbethi非典型记忆B细胞的扩增。

Malaria-induced interferon-γ drives the expansion of Tbethi atypical memory B cells.

作者信息

Obeng-Adjei Nyamekye, Portugal Silvia, Holla Prasida, Li Shanping, Sohn Haewon, Ambegaonkar Abhijit, Skinner Jeff, Bowyer Georgina, Doumbo Ogobara K, Traore Boubacar, Pierce Susan K, Crompton Peter D

机构信息

Malaria Infection Biology and Immunity Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America.

Center for Infectious Diseases, Parasitology, Heidelberg University Hospital, Heidelberg, Germany.

出版信息

PLoS Pathog. 2017 Sep 27;13(9):e1006576. doi: 10.1371/journal.ppat.1006576. eCollection 2017 Sep.

DOI:10.1371/journal.ppat.1006576
PMID:28953967
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5633206/
Abstract

Many chronic infections, including malaria and HIV, are associated with a large expansion of CD21-CD27- 'atypical' memory B cells (MBCs) that exhibit reduced B cell receptor (BCR) signaling and effector functions. Little is known about the conditions or transcriptional regulators driving atypical MBC differentiation. Here we show that atypical MBCs in malaria-exposed individuals highly express the transcription factor T-bet, and that T-bet expression correlates inversely with BCR signaling and skews toward IgG3 class switching. Moreover, a longitudinal analysis of a subset of children suggested a correlation between the incidence of febrile malaria and the expansion of T-bethi B cells. The Th1-cytokine containing supernatants of malaria-stimulated PBMCs plus BCR cross linking induced T-bet expression in naïve B cells that was abrogated by neutralizing IFN-γ or blocking the IFN-γ receptor on B cells. Accordingly, recombinant IFN-γ plus BCR cross-linking drove T-bet expression in peripheral and tonsillar B cells. Consistent with this, Th1-polarized Tfh (Tfh-1) cells more efficiently induced T-bet expression in naïve B cells. These data provide new insight into the mechanisms underlying atypical MBC differentiation.

摘要

许多慢性感染，包括疟疾和艾滋病病毒，都与CD21-CD27-“非典型”记忆B细胞（MBC）的大量扩增有关，这些细胞表现出降低的B细胞受体（BCR）信号传导和效应功能。关于驱动非典型MBC分化的条件或转录调节因子知之甚少。在这里，我们表明，接触疟疾个体中的非典型MBC高度表达转录因子T-bet，并且T-bet表达与BCR信号传导呈负相关，并倾向于IgG3类别转换。此外，对一部分儿童的纵向分析表明，发热性疟疾的发病率与T-bet高表达B细胞的扩增之间存在相关性。疟疾刺激的外周血单核细胞（PBMC）加上BCR交联的含Th1细胞因子的上清液可诱导幼稚B细胞中T-bet的表达，而中和IFN-γ或阻断B细胞上的IFN-γ受体可消除这种表达。因此，重组IFN-γ加上BCR交联可驱动外周和扁桃体B细胞中T-bet的表达。与此一致的是，Th1极化的滤泡辅助性T细胞（Tfh-1）能更有效地诱导幼稚B细胞中T-bet的表达。这些数据为非典型MBC分化的潜在机制提供了新的见解。

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