Osteoblasts and perivascular stromal cells constitute essential niches for HSC self-renewal and maintenance in the bone marrow. Wnt signaling is important to maintain HSC integrity. However, the paracrine role of Wnt proteins in osteoblasts-supported HSC maintenance and differentiation remains unclear. Here, we investigated hematopoiesis in mice with Wntless (Wls) deficiency in osteoblasts or Nestin-positive mesenchymal progenitor cells, which presumptively block Wnt secretion in osteoblasts. We detected defective B-cell lymphopoiesis and abnormal T-cell infiltration in the bone marrow of Wls mutant mice. Notably, no impact on HSC frequency and repopulation in the bone marrow was observed with the loss of osteoblastic Wls. Our findings revealed a supportive role of Wnts in osteoblasts-regulated B-cell lymphopoiesis. They also suggest a preferential niche role of osteoblastic Wnts for lymphoid cells rather than HSCs, providing new clues for the molecular nature of distinct niches occupied by different hematopoietic cells.

中文翻译：

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骨膜内壁ni的Wntless消融会损害淋巴细胞生成能力，而不是HSC的维持能力。

成骨细胞和血管周间质细胞构成了HSC自我更新和维持骨髓的重要功能。Wnt信号对于维持HSC完整性很重要。然而，Wnt蛋白在成骨细胞支持的HSC维持和分化中的旁分泌作用仍不清楚。在这里，我们调查了成骨细胞或Nestin阳性间充质祖细胞中具有Wntless（Wls）缺乏症的小鼠的造血作用，推测这可能会阻止成骨细胞中Wnt的分泌。我们在Wls突变小鼠的骨髓中检测到缺陷的B细胞淋巴细胞生成和异常的T细胞浸润。值得注意的是，由于成骨细胞Wls的丧失，未观察到对HSC频率和骨髓中再繁殖的影响。我们的发现揭示了Wnts在成骨细胞调节的B细胞淋巴细胞生成中的支持作用。