CD4+CD3- cells are the predominant hematopoietic cells found in mouse fetal intestine. We prove their role as Peyer's patch (PP)-inducing cells by transfer into neonatal PP-deficient mice. To test the requirement of chemokines and adhesion molecules in induction of PP, we studied mice deficient in CXCR5 and/or alpha4beta1 integrin-mediated adhesion. CXCR5-/- mice have CD4+CD3- cells, which are inefficient in inducing PP formation. We show here that CXCR5/CXCL13 signaling activates alpha4beta1 integrin on CD4+CD3- cells. Blocking of beta1 integrin or VCAM-1, the ligand of alpha4beta1 integrin, inhibits PP formation. This study demonstrates the link between chemokine receptors and adhesion molecules that regulates stromal/hematopoietic cell interaction leading to PP formation.

中文翻译：

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CD4 + CD3-细胞诱导Peyer斑的形成：CXCR5激活alpha4beta1整合素的作用。

CD4 + CD3-细胞是在小鼠胎儿肠道中发现的主要造血细胞。我们通过转移到新生儿PP缺陷型小鼠中证明了它们作为诱导Peyer's patch（PP）的细胞的作用。若要测试趋化因子和粘附分子诱导PP的需求，我们研究了CXCR5和/或alpha4beta1整合素介导的粘附缺陷的小鼠。CXCR5-/-小鼠具有CD4 + CD3-细胞，在诱导PP形成方面效率低下。我们在这里显示CXCR5 / CXCL13信号激活CD4 + CD3-细胞上的alpha4beta1整合素。beta1整合素或VCAM-1（α4beta1整合素的配体）的阻滞抑制了PP的形成。这项研究证明了趋化因子受体与粘附分子之间的联系，后者调节基质/造血细胞之间的相互作用，从而导致PP的形成。