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Updated: Jun 20, 2026
09:51
Development and Functional Characterization of Murine Tolerogenic Dendritic Cells
Published on: May 18, 2018
Bacterial signalling overrides cytokine signalling and modifies dendritic cell differentiation
Julie M Davies1, Barbara Sheil, Fergus Shanahan
1Alimentary Pharmabiotic Centre, University College Cork, National University of Ireland, Cork, Ireland.
Immunology
|September 11, 2009
Summary
Commensal bacteria, like Lactobacillus and Bifidobacterium, significantly alter dendritic cell (DC) differentiation in the gut. This bacterial signaling, dependent on Myeloid differentiation factor 88 (MyD88), promotes immune tolerance by creating suppressive, monocyte-like DCs.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Dendritic cell (DC) heterogeneity in the gut is influenced by local environmental factors.
- Bacterial signaling is a key factor shaping immune cell development in the mucosa.
Purpose of the Study:
- To investigate the impact of commensal bacteria on dendritic cell (DC) differentiation and function.
- To elucidate the role of Toll-like receptor signaling in bacterial modulation of DCs.
Main Methods:
- Murine bone marrow progenitors were exposed to specific commensal bacteria (Lactobacillus salivarius, Bifidobacterium breve, Bifidobacterium infantis).
- Cell surface phenotype and function were analyzed.
- Myeloid differentiation factor 88 knockout (MyD88-/-) cells were used to assess Toll-like receptor pathway involvement.
Main Results:
- Commensal bacteria consistently inhibited DC differentiation in a dose-dependent manner, promoting a monocyte-like phenotype (Gr-1(+) CD11b(+)).
- Even a single bacterium could alter precursor cell phenotype.
- This effect was Myeloid differentiation factor 88 (MyD88)-dependent, indicating Toll-like receptor pathway activation.
- Enhanced interleukin-10 production and Forkhead box P3 expression correlated with reduced T-cell proliferation.
Conclusions:
- Enteric commensal bacteria signaling through pattern recognition receptors alters DC differentiation in early precursors.
- This process results in the generation of functionally suppressive, monocyte-like DCs.
- This mechanism likely contributes to mucosal immune tolerance towards the gut microbiota.
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