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Updated: May 23, 2026
09:51
Development and Functional Characterization of Murine Tolerogenic Dendritic Cells
Published on: May 18, 2018
ATG5 in DCs attenuates anti-malarial cellular immune responses through interfering with TLR2-mediated CD209A/DC-SIGN
Yongling Fan1, Shiming Jiao1, Hangyu Li1
1Department of Pathogenic Biology, Army Medical University (Third Military Medical University), Chongqing, China.
Autophagy
|May 22, 2026
Summary
Autophagy related 5 (ATG5) deficiency in dendritic cells (DCs) suppresses malaria parasite growth by enhancing CD4+ T cell responses. This occurs via increased DC-SIGN expression on DCs, modulated by toll-like receptor 2 signaling.
Area of Science:
- Immunology
- Cell Biology
- Parasitology
Background:
- Dendritic cell (DC) function is impaired during malaria infection, but mechanisms are unclear.
- Autophagy related 5 (ATG5) plays a role in cellular processes, but its specific function in DCs during malaria is unknown.
Purpose of the Study:
- To investigate the role of ATG5 in dendritic cells during malaria infection.
- To elucidate the mechanisms by which ATG5 deficiency affects anti-malarial immunity.
Main Methods:
- Used atg5Itgax/Cd11c-Cre+ mice to study ATG5 deficiency in DCs.
- Analyzed parasite growth, T cell responses (CD4+ and CD8+), and expression of DC-SIGN (CD209A) and toll-like receptor 2 (TLR2).
Main Results:
- ATG5 deficiency in DCs suppressed malaria blood-stage parasite growth independently of canonical autophagy.
- Reduced parasite growth correlated with enhanced Plasmodium-specific CD4+ T cell responses, supporting CD8+ T cell activation.
- ATG5 deficiency increased DC-SIGN expression on conventional DCs (cDCs) via augmented TLR2 signaling, enhancing CD4+ T cell activation.
Conclusions:
- ATG5 deficiency in DCs modulates anti-malarial immunity by enhancing TLR2-mediated DC-SIGN expression.
- This study reveals a novel role for ATG5 in regulating DC function and anti-malarial responses.
- Findings offer insights for developing improved malaria vaccines.
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