IFIBYNE   05513
INSTITUTO DE FISIOLOGIA, BIOLOGIA MOLECULAR Y NEUROCIENCIAS
Unidad Ejecutora - UE
artículos
Título:
Neutrophil Signaling Pathways Activated by Bacterial DNA
Autor/es:
ALVAREZ, M. E.; FUXMAN BASS, J. I.; GEFFNER, J. R.; FERNÁNDEZ CALOTTI, P. X.; COSTAS, M.; COSO, O. A.; GAMBERALE, R.; VERMEULEN, M. E.; SALAMONE, G.; MARTINEZ, D.; TANOS, T.; TREVANI, A. S.
Revista:
JOURNAL OF IMMUNOLOGY
Referencias:
Año: 2006 p. 4037 - 4046
ISSN:
0022-1767
Resumen:
Abstract
We have previously shown that bacterial DNA activates human neutrophils in a CpG-independent manner. In this study, we have
characterized the signaling pathways involved in the activation mechanism. We found that p38 MAPK, ERK1/2, and JNK
pathways, as well as the PI3K/Akt pathway, are activated by bacterial DNA. We also determined that bacterial DNA induces
NF-B and AP-1 activation. When analyzing the role of these pathways on neutrophil functions, we observed that up-regulation
of CD11b triggered by bacterial DNA was decreased by pharmacological inhibitors of the p38 MAPK, ERK1/2, and JNK, whereas
stimulation of IL-8 release was dependent on p38, ERK1/2, and NF-B. Moreover, we found that IL-8 production was markedly
enhanced by inhibition of JNK, suggesting that this pathway negatively modulates NF-B-dependent transcription. We also
observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined
that bacterial DNA stimulated CD11b up-regulation in TLR9/ but not in MyD88/ mouse neutrophils, supporting that
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
TLR9/
observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined
that bacterial DNA stimulated CD11b up-regulation in TLR9/ but not in MyD88/ mouse neutrophils, supporting that
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
TLR9/
observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined
that bacterial DNA stimulated CD11b up-regulation in TLR9/ but not in MyD88/ mouse neutrophils, supporting that
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
TLR9/
enhanced by inhibition of JNK, suggesting that this pathway negatively modulates NF-B-dependent transcription. We also
observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined
that bacterial DNA stimulated CD11b up-regulation in TLR9/ but not in MyD88/ mouse neutrophils, supporting that
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
TLR9/
observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined
that bacterial DNA stimulated CD11b up-regulation in TLR9/ but not in MyD88/ mouse neutrophils, supporting that
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
TLR9/
observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined
that bacterial DNA stimulated CD11b up-regulation in TLR9/ but not in MyD88/ mouse neutrophils, supporting that
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
TLR9/
enhanced by inhibition of JNK, suggesting that this pathway negatively modulates NF-B-dependent transcription. We also
observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined
that bacterial DNA stimulated CD11b up-regulation in TLR9/ but not in MyD88/ mouse neutrophils, supporting that
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
TLR9/
observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined
that bacterial DNA stimulated CD11b up-regulation in TLR9/ but not in MyD88/ mouse neutrophils, supporting that
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
TLR9/
observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined
that bacterial DNA stimulated CD11b up-regulation in TLR9/ but not in MyD88/ mouse neutrophils, supporting that
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
TLR9/
of CD11b triggered by bacterial DNA was decreased by pharmacological inhibitors of the p38 MAPK, ERK1/2, and JNK, whereas
stimulation of IL-8 release was dependent on p38, ERK1/2, and NF-B. Moreover, we found that IL-8 production was markedly
enhanced by inhibition of JNK, suggesting that this pathway negatively modulates NF-B-dependent transcription. We also
observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined
that bacterial DNA stimulated CD11b up-regulation in TLR9/ but not in MyD88/ mouse neutrophils, supporting that
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
TLR9/
observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined
that bacterial DNA stimulated CD11b up-regulation in TLR9/ but not in MyD88/ mouse neutrophils, supporting that
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
TLR9/
observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined
that bacterial DNA stimulated CD11b up-regulation in TLR9/ but not in MyD88/ mouse neutrophils, supporting that
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
TLR9/
enhanced by inhibition of JNK, suggesting that this pathway negatively modulates NF-B-dependent transcription. We also
observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined
that bacterial DNA stimulated CD11b up-regulation in TLR9/ but not in MyD88/ mouse neutrophils, supporting that
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
TLR9/
observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined
that bacterial DNA stimulated CD11b up-regulation in TLR9/ but not in MyD88/ mouse neutrophils, supporting that
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
TLR9/
observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined
that bacterial DNA stimulated CD11b up-regulation in TLR9/ but not in MyD88/ mouse neutrophils, supporting that
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
TLR9/
enhanced by inhibition of JNK, suggesting that this pathway negatively modulates NF-B-dependent transcription. We also
observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined
that bacterial DNA stimulated CD11b up-regulation in TLR9/ but not in MyD88/ mouse neutrophils, supporting that
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
TLR9/
observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined
that bacterial DNA stimulated CD11b up-regulation in TLR9/ but not in MyD88/ mouse neutrophils, supporting that
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
TLR9/
observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined
that bacterial DNA stimulated CD11b up-regulation in TLR9/ but not in MyD88/ mouse neutrophils, supporting that
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
TLR9/
of CD11b triggered by bacterial DNA was decreased by pharmacological inhibitors of the p38 MAPK, ERK1/2, and JNK, whereas
stimulation of IL-8 release was dependent on p38, ERK1/2, and NF-B. Moreover, we found that IL-8 production was markedly
enhanced by inhibition of JNK, suggesting that this pathway negatively modulates NF-B-dependent transcription. We also
observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined
that bacterial DNA stimulated CD11b up-regulation in TLR9/ but not in MyD88/ mouse neutrophils, supporting that
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
TLR9/
observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined
that bacterial DNA stimulated CD11b up-regulation in TLR9/ but not in MyD88/ mouse neutrophils, supporting that
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
TLR9/
observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined
that bacterial DNA stimulated CD11b up-regulation in TLR9/ but not in MyD88/ mouse neutrophils, supporting that
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
TLR9/
enhanced by inhibition of JNK, suggesting that this pathway negatively modulates NF-B-dependent transcription. We also
observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined
that bacterial DNA stimulated CD11b up-regulation in TLR9/ but not in MyD88/ mouse neutrophils, supporting that
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. The Journal of
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
Immunology, 2006, 177: 40374046.
The Journal of
Immunology, 2006, 177: 40374046.2006, 177: 40374046.
TLR9/
observed that bacterial DNA stimulated IL-