CpG DNA induces self and cross-hyporesponsiveness of RAW264.7 cells in response to CpG DNA and lipopolysaccharide: Alterations in IL-1 receptor-associated kinase expression

Seon Ju Yeo, Jae Geun Yoon, Soon Cheol Hong, Ae-Kyung Yi

Research output: Contribution to journalArticle

93 Citations (Scopus)

Abstract

Exposure of macrophages to LPS induces a state of hyporesponsiveness to subsequent challenge with LPS. It has not been known whether previous exposure to CpG DNA induces a similar suppressive response to subsequent stimulation with CpG DNA. In the present study, we demonstrate that pretreatment with CpG DNA induces suppression of cytokine release in a murine macrophage-like cell RAW264.7 in response to subsequent challenge by CpG DNA. Additionally, CpG DNA-mediated activation of mitogen-activated protein kinases, including c-Jun NH2-terminal kinase, extracellular signal-regulated kinase, and p38, and activation of transcription factors AP-1, CREB, NF-κB, and STAT1 are greatly suppressed in the cells pre-exposed to CpG DNA. Pretreatment with CpG DNA also partially inhibited LPS-mediated production of cytokines and activation of mitogen-activated protein kinases and transcription factors. Neither LPS nor CpG DNA treatment inhibited Toll-like receptor 4, MD2, Toll-like receptor 9, myeloid differentiation factor 88, Toll/IL-1R domain-containing adaptor protein, Tollip, and TNF-α receptor-associated factor 6 expression. Interestingly, CpG DNA or LPS stimulation led to the inhibition of IL-1R-associated kinase expression. These results indicate that CpG DNA-induced refractory of RAW264.7 cells may be, at least in part, due to suppressed IL-1R-associated kinase expression.

Original languageEnglish (US)
Pages (from-to)1052-1061
Number of pages10
JournalJournal of Immunology
Volume170
Issue number2
DOIs
StatePublished - Jan 15 2003

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Interleukin-1 Receptor-Associated Kinases
Lipopolysaccharides
DNA
Mitogen-Activated Protein Kinases
Phosphotransferases
Myeloid Differentiation Factor 88
TNF Receptor-Associated Factor 6
Macrophages
Toll-Like Receptor 9
Cytokines
Toll-Like Receptor 4
JNK Mitogen-Activated Protein Kinases
Extracellular Signal-Regulated MAP Kinases
Transcription Factor AP-1
Transcription Factors

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

Cite this

CpG DNA induces self and cross-hyporesponsiveness of RAW264.7 cells in response to CpG DNA and lipopolysaccharide : Alterations in IL-1 receptor-associated kinase expression. / Yeo, Seon Ju; Yoon, Jae Geun; Hong, Soon Cheol; Yi, Ae-Kyung.

In: Journal of Immunology, Vol. 170, No. 2, 15.01.2003, p. 1052-1061.

Research output: Contribution to journalArticle

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abstract = "Exposure of macrophages to LPS induces a state of hyporesponsiveness to subsequent challenge with LPS. It has not been known whether previous exposure to CpG DNA induces a similar suppressive response to subsequent stimulation with CpG DNA. In the present study, we demonstrate that pretreatment with CpG DNA induces suppression of cytokine release in a murine macrophage-like cell RAW264.7 in response to subsequent challenge by CpG DNA. Additionally, CpG DNA-mediated activation of mitogen-activated protein kinases, including c-Jun NH2-terminal kinase, extracellular signal-regulated kinase, and p38, and activation of transcription factors AP-1, CREB, NF-κB, and STAT1 are greatly suppressed in the cells pre-exposed to CpG DNA. Pretreatment with CpG DNA also partially inhibited LPS-mediated production of cytokines and activation of mitogen-activated protein kinases and transcription factors. Neither LPS nor CpG DNA treatment inhibited Toll-like receptor 4, MD2, Toll-like receptor 9, myeloid differentiation factor 88, Toll/IL-1R domain-containing adaptor protein, Tollip, and TNF-α receptor-associated factor 6 expression. Interestingly, CpG DNA or LPS stimulation led to the inhibition of IL-1R-associated kinase expression. These results indicate that CpG DNA-induced refractory of RAW264.7 cells may be, at least in part, due to suppressed IL-1R-associated kinase expression.",
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