Requirement for DNA CpG Content in TLR9-Dependent Dendritic Cell Activation Induced by DNA-Containing Immune Complexes
Open accessAbstract
Although TLR9 was originally thought to specifically recognize microbial DNA, it is now evident that mammalian DNA can be an effective TLR9 ligand. However, the DNA sequence required for TLR9 activation is controversial, as studies have shown conflicting results depending on the nature of the DNA backbone, the route of DNA uptake, and the cell type being studied. In systemic lupus erythematosus, a major route whereby DNA gains access to intracellular TLR9, and thereby activates dendritic cells (DCs), is through uptake as a DNA-containing immune complex. In this report, we used defined dsDNA fragments with a natural (phosphodiester) backbone and show that unmethylated CpG dinucleotides within dsDNA are required for murine DC TLR9 activation induced by a DNA-containing immune complex. The strongest activation is seen with dsDNA fragments containing optimal CpG motifs (purine-purine-CpG-pyrimidine-pyrimidine) that are common in microbial DNA but rare in mammalian DNA. Importantly, however, activation can also be induced by CpG-rich DNA fragments that lack these optimal CpG motifs and that we show are plentiful in CpG islands within mammalian DNA. No activation is induced by DNA fragments lacking CpG dinucleotides, although this CpG-free DNA can induce DC activation if internalized by liposomal transfection instead of as an immune complex. Overall, the data suggest that the release of CpG-rich DNA from mammalian DNA may contribute to the pathogenesis of autoimmune diseases such as systemic lupus erythematosus and psoriasis in which activation of TLR9 in DCs by self DNA has been implicated in disease pathogenesis.
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This innate immune activation promotes dendritic cell maturation and enhances antigen processing and presentation via MHC class I and II pathways.
“This innate immune activation promotes dendritic cell maturation and enhances antigen processing and presentation via major histocompatibility complex (MHC) class I and II pathways [75]”
From Phage therapy in oncology: opportunities for cancer prevention and treatment (2026) · cites this paper as [75]
The Results (page unavailable in our copy) show that CpG-containing DNA immune complexes activate dendritic cells through TLR9, inducing cytokine production and upregulation of the co-stimulatory molecule CD40. This supports dendritic-cell activation consistent with maturation, but the paper does not show enhanced antigen processing or presentation through MHC class I or II pathways. (LLM, conf=0.88)
Experimental — accuracy not yet measuredFollowing endocytic uptake by antigen-presenting cells, phage DNA traffics to endosomal compartments, where acidification and partial degradation of double-stranded DNA into single-stranded fragments expose CpG motifs for recognition by TLR9.
“Following endocytic uptake by antigen-presenting cells, including plasmacytoid dendritic cells, macrophages, and B cells, phage DNA traffics to endosomal compartments, where acidification and partial degradation of double-stranded DNA into single-stranded fragments expose CpG motifs for recognition by Toll-like receptor 9 (TLR9) [75]”
From Phage therapy in oncology: opportunities for cancer prevention and treatment (2026) · cites this paper as [75]
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- Authors
- Yasuda, K., Richez, C., Uccellini, M. B., Richards, R. J., Bonegio, R. G., Akira, S., Monestier, M., Corley, R. B., Viglianti, G. A., Marshak-Rothstein, A., & Rifkin, I. R.
- Affiliations
- Renal Section, Department of Medicine
- Boston University (US)
- Research Institute for Microbial Diseases, The University of Osaka (JP)
- Temple University (US)
- Department of Microbiology, Boston University School of Medicine , Boston, MA 02118
- Corresponding author
- Yasuda, Kei
- Richez, Christophe
- ORCID
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-09-01
- Volume
- 183
- Issue
- 5
- Pages
- 3109-3117
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC2860771
- OpenAlex
- W1877684281
- Cited by
- 118
- References
- 62
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 1 · 2023: 2 · 2022: 1 · 2021: 9 · 2020: 8 · 2019: 7 · 2018: 6 · 2017: 8 · 2016: 9 · 2015: 9 · 2014: 8 · 2013: 9 · 2012: 9
- FWCI
- 4.60
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR050256, P01AR050256)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- TLR9, dendritic cell activation, CpG, self-DNA, systemic lupus erythematosus, psoriasis, CpG islands, double-stranded DNA, liposomal transfection, DNA uptake, autoimmune disease pathogenesis
- MeSH terms
- Adjuvants, Immunologic, Animals, Antigen-Antibody Complex, Cells, Cultured, Dendritic Cells, DNA, Humans, Lupus Erythematosus, Systemic, Mice, Inbred BALB C, Psoriasis, Mice, Knockout, CpG Islands, DNA Methylation, Toll-Like Receptor 9, Mice, DNA Fragmentation, Phosphorothioate Oligonucleotides
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