Cutting Edge: Role of Toll-Like Receptor 9 in CpG DNA-Induced Activation of Human Cells

Unmethylated CpG motifs present in bacterial DNA stimulate a rapid and robust innate immune response. Human cell lines and PBMC that recognize CpG DNA express membrane-bound human Toll-like receptor 9 (hTLR9). Cells that are not responsive to CpG DNA become responsive when transfected with hTLR9. Ex...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2001-10, Vol.167 (7), p.3555-3558
Main Authors: Takeshita, Fumihiko, Leifer, Cynthia A, Gursel, Ihsan, Ishii, Ken J, Takeshita, Saoko, Gursel, Mayda, Klinman, Dennis M
Format: Article
Language:English
Subjects:
Cell Line
Cells, Cultured
CpG Islands
DNA-Binding Proteins - chemistry
DNA-Binding Proteins - genetics
DNA-Binding Proteins - physiology
Humans
Interleukin-1 Receptor-Associated Kinases
Jurkat Cells
Oligodeoxyribonucleotides - pharmacology
Protein Kinases - physiology
Protein Structure, Tertiary
Proteins - physiology
Receptors, Cell Surface - chemistry
Receptors, Cell Surface - genetics
Receptors, Cell Surface - physiology
RNA, Messenger - biosynthesis
Signal Transduction
TNF Receptor-Associated Factor 6
Toll-Like Receptor 9
Transfection
Transport Vesicles - chemistry
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Summary:Unmethylated CpG motifs present in bacterial DNA stimulate a rapid and robust innate immune response. Human cell lines and PBMC that recognize CpG DNA express membrane-bound human Toll-like receptor 9 (hTLR9). Cells that are not responsive to CpG DNA become responsive when transfected with hTLR9. Expression of hTLR9 dramatically increases uptake of CpG (but not control) DNA into endocytic vesicles. Upon cell stimulation, hTLR9 and CpG DNA are found in the same endocytic vesicles. Cells expressing hTLR9 are stimulated by CpG motifs that are active in primates but not rodents, suggesting that evolutionary divergence between TLR9 molecules underlies species-specific differences in the recognition of bacterial DNA. These findings indicate that hTLR9 plays a critical role in the CpG DNA-mediated activation of human cells.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.167.7.3555