| First Author | Gladow N | Year | 2024 |
| Journal | Basic Res Cardiol | Volume | 119 |
| Issue | 2 | Pages | 261-275 |
| PubMed ID | 38436707 | Mgi Jnum | J:360207 |
| Mgi Id | MGI:7705640 | Doi | 10.1007/s00395-024-01035-3 |
| Citation | Gladow N, et al. (2024) Role of CD4(+) T-cells for regulating splenic myelopoiesis and monocyte differentiation after experimental myocardial infarction. Basic Res Cardiol 119(2):261-275 |
| abstractText | 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-gamma) 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-gamma responsive genes after MI. Our results indicate that conventional CD4(+) T-cells promote and Tregs attenuate splenic myelopoiesis and proinflammatory differentiation of monocytes. |
