CD11c+ Cells Control Platelet Homeostasis in a Murine Bone Marrow Chimeric Atherosclerosis Model
Manuela Sauter1,2,3,4,5, Serena Gregori2,3,4,5, Harald F Langer1,2,3,4,5
1Helmholtz-Institute for Translational AngioCardioScience (HI-TAC), 68167 Mannheim, Germany.
Biomedicines
|February 27, 2026
Summary
Loss of CD11c+ cells in mice with atherosclerosis accelerates platelet production and increases circulating platelet counts, linked to elevated thrombopoietin and inflammatory signals.
Area of Science:
- Immunology
- Cardiovascular Disease
- Hematology
Background:
- Dendritic cells (DCs) are crucial immune regulators in cardiovascular disease.
- The role of DCs in platelet production and homeostasis is not fully understood.
- Previous work showed CD11c+ cell depletion accelerates atherosclerosis.
Purpose of the Study:
- To investigate if sustained CD11c+ cell loss impacts platelet production.
- To determine if CD11c+ cell loss affects systemic inflammation under atherogenic conditions.
Main Methods:
- Used CD11c-DTR bone marrow chimeric mice on an ApoE-/- background, fed a high-cholesterol diet.
- Administered diphtheria toxin to deplete CD11c+ cells over six weeks.
- Quantified platelet counts, analyzed serum cytokines/chemokines, and measured thrombopoietin (TPO) levels.
Main Results:
- Chronic CD11c+ cell depletion significantly increased circulating platelet counts.
- Observed broad inflammatory remodeling with elevated cytokines linked to megakaryopoiesis and platelet activation.
- Found significantly elevated serum TPO levels after CD11c+ cell depletion.
Conclusions:
- Loss of CD11c+ cells in this model promotes a pro-thrombopoietic state.
- Elevated platelet counts and systemic inflammation are associated with CD11c+ cell depletion.
- Identified a CD11c+ cell-TPO-platelet axis connecting immune regulation to platelet homeostasis in atherogenesis.
