ISSN: 2381-8727



当社グループは 3,000 以上の世界的なカンファレンスシリーズ 米国、ヨーロッパ、世界中で毎年イベントが開催されます。 1,000 のより科学的な学会からの支援を受けたアジア および 700 以上の オープン アクセスを発行ジャーナルには 50,000 人以上の著名人が掲載されており、科学者が編集委員として名高い

700 ジャーナル 15,000,000 人の読者 各ジャーナルは 25,000 人以上の読者を獲得


Prenatal Inflammation Disrupts Murine Foetal Hematopoietic Development and Alters Postnatal Immunity

Annie Beudin

Adult hematopoietic stem and progenitor cells (HSPCs) respond directly to inflammation and infection, changing their quiescence, mobilisation, and differentiation in both acute and chronic ways. We show that murine foetal HSPCs respond in utero to prenatal inflammation, and that this response shapes postnatal hematopoiesis and immune cell function. Divergent responses of heterogeneous foetal HSPCs to maternal immune activation (MIA) include changes in quiescence, expansion, and lineage-biased output [1 ]. In response to MIA, single-cell transcriptomic analysis of foetal HSPCs reveals specific upregulation of inflammatory gene profiles in discrete, transient hematopoietic stem cell (HSC) populations that propagate expansion of lymphoid-biased progenitors. MIA causes inappropriate postnatal expansion and persistence of foetal lymphoid-biased progenitors, as well as increased cellularity and hyperresponsiveness of fetal-derived innate-like lymphocytes. By reshaping foetal HSC establishment, we show how inflammation in utero can direct the output and function of fetal-derived immune cells [2].