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Updated: Mar 25, 2026

Development and Functional Characterization of Murine Tolerogenic Dendritic Cells
Published on: May 18, 2018
Energy restriction impairs dendritic cell development in C57BL/6J mice
David M Duriancik1, Elizabeth M Gardner1
1Department of Food Science & Human Nutrition, Michigan State University, East Lansing, MI 48824-1224, United States.
Energy restriction (ER) in mice reduces dendritic cell (DC) development while increasing myeloid progenitors and macrophages. This dietary intervention alters immune cell populations, potentially impacting responses to infection.
Area of Science:
- Immunology
- Cell Biology
- Dietary Interventions
Background:
- Dendritic cells (DCs) are crucial antigen-presenting cells that initiate T lymphocyte responses.
- Energy restriction (ER) is a dietary intervention linked to longevity but with complex effects on immunity.
- Understanding DC development under ER is vital for assessing immune function.
Purpose of the Study:
- To investigate the impact of a 40% energy restriction (ER) diet on dendritic cell development in adult C57Bl6J mice.
- To analyze changes in myeloid progenitors, DC subsets, and related immune cells in the bone marrow of ER-fed mice.
Main Methods:
- Adult C57Bl6J mice were fed a 40% ER diet or an ad libitum (AL) diet.
- Flow cytometry was used to analyze bone marrow cell populations, including myeloid progenitors and DC subsets.
- Proliferation rates were assessed using BrdU incorporation and Ki-67 staining.
Main Results:
- ER mice exhibited increased myeloid progenitors but decreased common DC progenitors, precursor conventional DCs, and plasmacytoid DCs.
- A rise in macrophages and CD169+ cells was observed in the bone marrow of ER mice.
- In vitro culture with GM-CSF or Flt3L did not reveal significant differences in DC subsets, suggesting proliferation rates are key.
Conclusions:
- Energy restriction alters myelopoiesis, leading to reduced dendritic cell development and enhanced monocyte/macrophage development in steady-state mice.
- These findings may explain previously observed impaired innate immune responses to primary infections, like influenza, in ER-fed mice.
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