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Journalartikel - Wissenschaftlicher Artikel | Open Access

Role of CD4⁺ T-Cells for Regulating Splenic Myelopoiesis and Monocyte Differentiation after Experimental Myocardial Infarction

Autor*innen
Gladow, Nadine ; Hollmann, Claudia ; Weirather, Johannes ; Ding, Xin ; Burkard, Matthias ; Uehlein, Sabrina ; Bharti, Richa ; Förstner, Konrad ; Kerkau, Thomas ; Beyersdorf, Niklas ; Frantz, Stefan ; Ramos, Gustavo ; Hofmann, Ulrich
Zeitschrift
Basic research in cardiology 
DOI
10.1007/s00395-024-01035-3

Weitere Details

Sprache
englisch
Darstellungsform
Text
Schlüsselwörter
Lymphocytes , Monocytes , Myocardial Infarction , Treg

Myocardial infarction (MI) induces the generation of proinflammatory Ly6Chⁱgh 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 Ly6Chⁱgh 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.

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