Myocardial infarction (MI) induces the generation of proinflammatory Ly6C^high monocytes in the spleen and the recruitment of these cells to the myocardium. CD4⁺ Foxp3⁺ CD25⁺ T-cells (Tregs) promote the healing process after myocardial infarction by engendering a pro-healing differentiation state in myocardial monocyte-derived macrophages. We aimed to study the effects of CD4⁺ T-cells on splenic myelopoiesis and monocyte differentiation. We instigated MI in mice and found that MI-induced splenic myelopoiesis is abrogated in CD4⁺ T-cell deficient animals. Conventional CD4⁺ T-cells promoted myelopoiesis in vitro by cell–cell-contact and paracrine mechanisms, including interferon-gamma (IFN-γ) signalling. Depletion of regulatory T-cells enhanced myelopoiesis in vivo, as evidenced by increases in progenitor cell numbers and proliferative activity in the spleen 5 days after MI. The frequency of CD4⁺ T-cells-producing factors that promote myelopoiesis increased within the spleen of Treg-depleted mice. Moreover, depletion of Tregs caused a proinflammatory bias in splenic Ly6C^high monocytes, which showed predominantly upregulated expression of IFN-γ responsive genes after MI. Our results indicate that conventional CD4⁺ T-cells promote and Tregs attenuate splenic myelopoiesis and proinflammatory differentiation of monocytes.

心肌梗塞 (MI) 会诱导脾脏中促炎性 Ly6C^高单核细胞的产生，并将这些细胞募集至心肌。 CD4 ⁺ Foxp3 ⁺ CD25 ⁺ T 细胞 (Treg) 通过在心肌单核细胞衍生的巨噬细胞中产生促愈合分化状态来促进心肌梗死后的愈合过程。我们的目的是研究 CD4 ⁺ T 细胞对脾脏骨髓细胞生成和单核细胞分化的影响。我们对小鼠进行了 MI 实验，发现 MI 诱导的脾脏骨髓细胞生成在 CD4 ⁺ T 细胞缺陷的动物中被消除。传统的 CD4 ⁺ T 细胞通过细胞-细胞接触和旁分泌机制（包括干扰素-γ (IFN-γ) 信号传导）在体外促进骨髓生成。调节性 T 细胞的耗竭增强了体内骨髓生成，MI 后 5 天脾脏中祖细胞数量和增殖活性的增加证明了这一点。Treg 缺失小鼠脾脏中促进骨髓细胞生成的CD4 ⁺ T 细胞生成因子的频率增加。此外，Tregs 的消耗导致脾 Ly6C^高单核细胞出现促炎倾向，这表明 MI 后 IFN-γ 反应基因的表达主要上调。我们的结果表明，传统的 CD4 ⁺ T 细胞促进而 Tregs 减弱脾脏骨髓细胞生成和单核细胞的促炎分化。