The DNA binding protein AT-rich interacting domain 3a (ARID3a)² is expressed in healthy human hematopoietic cord blood progenitors where its modulation influences myeloid versus B lineage development. ARID3a is also variably expressed in subsets of adult peripheral blood hematopoietic progenitors where the consequences of ARID3a expression are unknown. In B lymphocytes, Toll-like receptor (TLR)³ signaling induces ARID3a expression in association with Type I interferon inflammatory cytokines. We hypothesized that TLR ligand stimulation of peripheral blood hematopoietic progenitors would induce ARID3a expression resulting in interferon production, and potentially influencing lineage decisions. Our data revealed that the TLR9 agonist CpG induces ARID3a expression with interferon alpha synthesis in human hematopoietic progenitors. However, ARID3a expression was not associated with increased B lineage development. These results demonstrate the need for further experiments to better define how pathogen-associated responses influence hematopoiesis.

DNA 结合蛋白富含 AT 的相互作用结构域 3a (ARID3a) ²在健康的人类造血脐带血祖细胞中表达，其调节影响骨髓与 B 谱系的发育。 ARID3a 在成人外周血造血祖细胞亚群中也有不同的表达，其中 ARID3a 表达的后果尚不清楚。在 B 淋巴细胞中，Toll 样受体 (TLR) ³信号传导诱导与 I 型干扰素炎症细胞因子相关的 ARID3a 表达。我们假设 TLR 配体刺激外周血造血祖细胞会诱导 ARID3a 表达，导致干扰素产生，并可能影响谱系决策。我们的数据显示，TLR9 激动剂 CpG 在人类造血祖细胞中诱导 ARID3a 表达以及干扰素 α 合成。然而，ARID3a 表达与 B 谱系发育增加无关。这些结果表明需要进一步的实验来更好地确定病原体相关反应如何影响造血。