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Updated: Feb 14, 2026

Isolation and Characterization of Dendritic Cells and Macrophages from the Mouse Intestine
Published on: May 21, 2012
Functional CD169 on Macrophages Mediates Interaction with Dendritic Cells for CD8+ T Cell Cross-Priming
Dieke van Dinther1, Henrike Veninga1, Salvador Iborra2
1Cancer Center Amsterdam, Department of Molecular Cell Biology and Immunology, VU University Medical Center, Amsterdam, the Netherlands.
Insights
Splenic CD169+ macrophages and CD8α+ dendritic cells collaborate to initiate CD8+ T cell responses. This interaction, crucial for immunity, relies on CD169 binding to sialic acids on dendritic cells.
Area of Science:
- Immunology
- Cell Biology
- Microbiology
Background:
- Splenic CD169+ macrophages capture blood-borne pathogens in the marginal zone.
- CD8+ T cell responses are critical for adaptive immunity against various infections.
Purpose of the Study:
- Investigate the requirements for CD169+ macrophage-mediated induction of CD8+ T cell responses.
- Elucidate the role of CD169 and CD8α+ dendritic cells in antigen presentation and T cell activation.
Main Methods:
- Antigen targeting to CD169+ macrophages.
- Analysis of T cell priming and activation.
- Assessment of CD169 binding capacity and functional relevance.
Main Results:
- BATF3-dependent CD8α+ dendritic cells are essential for DNGR-1-mediated CD8+ T cell cross-priming.
- CD169 preferentially binds to CD8α+ dendritic cells via sialic acid.
- CD169's sialic acid-binding capacity is critical for antigen transfer and T cell activation.
- Functional CD169 enhances CD8+ T cell responses during modified vaccinia Ankara virus infection.
Conclusions:
- CD169+ macrophages and CD8α+ dendritic cells collaborate for effective CD8+ T cell responses.
- CD169-sialic acid interaction facilitates antigen transfer and T cell activation, crucial for cellular immunity.
Abstract:
Splenic CD169+ macrophages are located in the marginal zone to efficiently capture blood-borne pathogens. Here, we investigate the requirements for the induction of CD8+ T cell responses by antigens (Ags) bound by CD169+ macrophages. Upon Ag targeting to CD169+ macrophages, we show that BATF3-dependent CD8α+ dendritic cells (DCs) are crucial for DNGR-1-mediated cross-priming of CD8+ T cell responses. In addition, we demonstrate that CD169, a sialic acid binding lectin involved in cell-cell contact, preferentially binds to CD8α+ DCs and that Ag transfer to CD8α+ DCs and subsequent T cell activation is dependent on the sialic acid-binding capacity of CD169. Finally, functional CD169 mediates optimal CD8+ T cell responses to modified vaccinia Ankara virus infection. Together, these data indicate that the collaboration of CD169+ macrophages and CD8α+ DCs for the initiation of effective CD8+ T cell responses is facilitated by binding of CD169 to sialic acid containing ligands on CD8α+ DCs.
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