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对抗原的有限接触促进早期B细胞记忆的产生
作者:小柯机器人 发布时间:2021/9/19 22:49:07

瑞典卡罗琳斯卡大学Taras Kreslavsky研究组发现,对抗原的有限接触促进早期B细胞记忆的产生,同时抑制浆母细胞反应。该研究于2021年9月14日发表于国际一流学术期刊《免疫》。

研究人员通过单细胞RNA测序研究了小鼠对T依赖性抗原的早期B细胞反应。免疫后的早期,一个均匀的活化前体(AP)群体产生了一波短暂的浆细胞(PB),一天后出现了生殖中心B细胞(GCBC)。大多数AP迅速退出细胞周期,产生了非GC衍生的早期记忆B细胞(eMBC),保留了类似AP的转录特征。

抗原可用性的迅速下降控制了这些事件;提供过量的抗原阻止了细胞周期的退出,并诱发了新一轮的B细胞。命运图谱显示了eMBC对MBC池的突出贡献。具有MBC表型的静止细胞在灵长类动物对免疫的早期反应中起主导作用。当未能控制威胁而表现为抗原的增加时,AP/eMBC的储备可能使免疫反应迅速重新调整。

据介绍,早期B细胞激活期间的细胞命运决定了对病原体和疫苗反应的结果。

附:英文原文

Title: Limited access to antigen drives generation of early B cell memory while restraining the plasmablast response

Author: Vassilis Glaros, René Rauschmeier, Artem V. Artemov, Annika Reinhardt, Sebastian Ols, Aikaterini Emmanouilidi, Charlotte Gustafsson, Yuanyuan You, Claudio Mirabello, sa K. Bjrklund, Laurent Perez, Neil P. King, Robert Mnsson, Davide Angeletti, Karin Loré, Igor Adameyko, Meinrad Busslinger, Taras Kreslavsky

Issue&Volume: 2021/09/14

Abstract: Cell fate decisions during early B cell activation determine the outcome of responses to pathogens and vaccines. We examined the early B cell response to T-dependent antigen in mice by single-cell RNA sequencing. Early after immunization, a homogeneous population of activated precursors (APs) gave rise to a transient wave of plasmablasts (PBs), followed a day later by the emergence of germinal center B cells (GCBCs). Most APs rapidly exited the cell cycle, giving rise to non-GC-derived early memory B cells (eMBCs) that retained an AP-like transcriptional profile. Rapid decline of antigen availability controlled these events; provision of excess antigen precluded cell cycle exit and induced a new wave of PBs. Fate mapping revealed a prominent contribution of eMBCs to the MBC pool. Quiescent cells with an MBC phenotype dominated the early response to immunization in primates. A reservoir of APs/eMBCs may enable rapid readjustment of the immune response when failure to contain a threat is manifested by increased antigen availability.

DOI: 10.1016/j.immuni.2021.08.017

Source: https://www.cell.com/immunity/fulltext/S1074-7613(21)00349-6

期刊信息

Immunity:《免疫》,创刊于1994年。隶属于细胞出版社,最新IF:21.522
官方网址:https://www.cell.com/immunity/home
投稿链接:https://www.editorialmanager.com/immunity/default.aspx