PMID: 14552837 Consistent with this, the proliferative response of bone-marrow-derived macrophages (BMMs) to colony-stimulating factor 1 [CSF1 or macrophage colony-stimulating factor (M-CSF)] was increased in IFNAR1¡Ý/¡Ý cells, as expected from the removal of an inhibitor of proliferation.

PMID: 14552837 This is followed by the recruitment and activation of IRAK and TRAF6.

PMID: 14552837 This is followed by the recruitment and activation of IRAK and TRAF6.

PMID: 14552837 This is followed by the recruitment and activation of IRAK and TRAF6.

PMID: 14552837 This is followed by the recruitment and activation of IRAK and TRAF6.

PMID: 14552837 This results in the activation of both the MAP kinases and NF-kappaB.

PMID: 14552837, 12471095, 12539043 Although previous studies would lead us to interpret data from overexpression or dominant-negative experiments with caution, the data on TLR3 activation of IFN-beta by TRIF/TICAM, but not by MyD88 or Mal/TIRAP, is consistent between these studies.

PMID: 14552837 This results in the activation of both the MAP kinases and NF-kappaB. PMID: 14552837 Recent studies demonstrated that IKbeta kinases, previously known to be involved in NF-kappaB activation, are essential for activation of IRF3 and 7.

PMID: 14552837, 11257452 LPS effects are mediated by the products of TLR response genes (TRGs), such as inducible nitric oxide synthase (NOS2), which generates microbicidal nitric oxide (NO) and cytokines such as interleukin-6 (IL-6), tumor necrosis factor-greek small letter alpha (TNF-alpha), interferons (IFNs) and chemokines.

PMID: 14552837, 11257452 LPS effects are mediated by the products of TLR response genes (TRGs), such as inducible nitric oxide synthase (NOS2), which generates microbicidal nitric oxide (NO) and cytokines such as interleukin-6 (IL-6), tumor necrosis factor-greek small letter alpha (TNF-alpha), interferons (IFNs) and chemokines.

PMID: 14552837, 12471095, 12539043 Although previous studies would lead us to interpret data from overexpression or dominant-negative experiments with caution, the data on TLR3 activation of IFN-beta by TRIF/TICAM, but not by MyD88 or Mal/TIRAP, is consistent between these studies.

PMID: 14552837, 8783497 Furthermore, IFN-beta itself can regulate the differentiation or activation of almost all effector cells of the immune system, including B cells and DCs.

PMID: 14552837, 12471095, 12539043 Although previous studies would lead us to interpret data from overexpression or dominant-negative experiments with caution, the data on TLR3 activation of IFN-beta by TRIF/TICAM, but not by MyD88 or Mal/TIRAP, is consistent between these studies. PMID: 14552837 However, in response to double-stranded RNA (poly I:C) activation of a related TLR3 receptor, the TRIF?TIR-containing adaptor molecule (TICAM) leads to IRF3 activation.

PMID: 14552837, 12471095, 12539043 Although previous studies would lead us to interpret data from overexpression or dominant-negative experiments with caution, the data on TLR3 activation of IFN-beta by TRIF/TICAM, but not by MyD88 or Mal/TIRAP, is consistent between these studies. PMID: 14552837 First, activation of IRF3 generated IFN-beta and -alpha4. PMID: 14552837, 11698465 Recent analyses of TLR signaling have identified the LPS induction of additional IFN response genes (IRGs), including IFN-gamma-inducible protein 10 (IP-10), monocyte chemotactic protein 5 (MCP-5), RANTES and IFN-stimulated gene 15 (ISG15), as well as IFN-beta through a so-called MyD88-independent pathway.

PMID: 14552837 First, activation of IRF3 generated IFN-beta and -alpha4.

PMID: 14552837 These acted through their cognate receptors, IFNAR1 and IFNAR2, to activate STAT1 to induce IRF7.

PMID: 14552837 These acted through their cognate receptors, IFNAR1 and IFNAR2, to activate STAT1 to induce IRF7.

PMID: 14552837 These acted through their cognate receptors, IFNAR1 and IFNAR2, to activate STAT1 to induce IRF7.

PMID: 14552837 These acted through their cognate receptors, IFNAR1 and IFNAR2, to activate STAT1 to induce IRF7.

PMID: 14552837 These acted through their cognate receptors, IFNAR1 and IFNAR2, to activate STAT1 to induce IRF7.

PMID: 14552837 Activation of IRF7 then induced the remaining IFN-alpha subtype.

PMID: 14552837 Recent studies demonstrated that IKbeta kinases, previously known to be involved in NF-kappaB activation, are essential for activation of IRF3 and 7.

PMID: 14552837 Activation of IRF7 then induced the remaining IFN-alpha subtype.

PMID: 14552837 Recent studies demonstrated that IKbeta kinases, previously known to be involved in NF-kappaB activation, are essential for activation of IRF3 and 7.

PMID: 14552837, 12062447 Similar studies indicated that Mal was necessary for the activation of IRF3 by LPS but not by poly I:C.

PMID: 14552837, 11698465 Recent analyses of TLR signaling have identified the LPS induction of additional IFN response genes (IRGs), including IFN-gamma-inducible protein 10 (IP-10), monocyte chemotactic protein 5 (MCP-5), RANTES and IFN-stimulated gene 15 (ISG15), as well as IFN-beta through a so-called MyD88-independent pathway.

PMID: 14552837, 11052814 We then demonstrated that LPS induction of NOS2 [22] and cyclin D2 [23] was also absent in IFNAR1¡Ý/¡Ý cells.

PMID: 14552837 Consistent with this, the proliferative response of bone-marrow-derived macrophages (BMMs) to colony-stimulating factor 1 [CSF1 or macrophage colony-stimulating factor (M-CSF)] was increased in IFNAR1¡Ý/¡Ý cells, as expected from the removal of an inhibitor of proliferation.

PMID: 14552837, 11698465 Recent analyses of TLR signaling have identified the LPS induction of additional IFN response genes (IRGs), including IFN-gamma-inducible protein 10 (IP-10), monocyte chemotactic protein 5 (MCP-5), RANTES and IFN-stimulated gene 15 (ISG15), as well as IFN-beta through a so-called MyD88-independent pathway.

PMID: 14552837, 11698465 Recent analyses of TLR signaling have identified the LPS induction of additional IFN response genes (IRGs), including IFN-gamma-inducible protein 10 (IP-10), monocyte chemotactic protein 5 (MCP-5), RANTES and IFN-stimulated gene 15 (ISG15), as well as IFN-beta through a so-called MyD88-independent pathway.