ライフサイエンスコーパス: TREM-1

1 ering Receptor-1 Expressed on Myeloid cells (TREM-1).

2 ntrol and implicate a novel biologic target (TREM-1).

3 2 species' subsets, including CD36, CD9, and TREM-1.

4 ted with HIV show an increased expression of TREM-1.

5 ith plasmid contenting wild type-promoter of TREM-1.

6 tion between the expression of TGF-beta1 and TREM-1.

7 The limits of detection of 3.3 pM for TREM-1, 1.1 nM for MMP-9 and 1.4 nM for HSL are either n

8 Unexpectedly, TREM-1/3 deficiency resulted in increased local and syst

9 model of pneumonia and found that absence of TREM-1/3 markedly increased mortality following Pseudomo

10 emotaxis; however, histologic examination of TREM-1/3-deficient lungs revealed decreased neutrophil i

11 We developed a TREM-1/3-deficient mouse model of pneumonia and found th

12 TREM-1/3-deficient neutrophils demonstrated intact bacte

13 TREM-1/3-deficient neutrophils effectively migrated acro

14 Humans have two forms of TREM-1: a membrane receptor, associated with the adaptor

15 TREM-1 activation also attenuates the induction of some

16 TREM-1 activation amplifies the Toll-like receptor initi

17 led analysis of the cellular consequences of TREM-1 activation and highlight the complexity in signal

18 ed, including SPP1 and CSF1 (i.e., M-CSF) by TREM-1 activation and IL-23 and CSF3 (i.e., G-CSF) by LP

19 Additionally, cross-talk between TREM-1 activation and LPS occurs on multiple levels.

20 Both TREM-1 activation and LPS up-regulate chemokines, cytoki

21 TREM-1 activation by receptor cross-linking has been sho

22 In primary human monocytes TREM-1 activation did not trigger innate antimicrobial p

23 mmune mediators including TLR signalling and TREM-1 activation of the inflammasome.

24 We propose that TREM-1 activation orchestrates monocyte/macrophage proin

25 LYRP1 bypassed the need for peptidoglycan in TREM-1 activation, demonstrating that the PGLYRP1/TREM-1

26 oluble form of TREM-1 (sTREM-1), a marker of TREM-1 activation, is detectable in the plasma of patien

27 To investigate the cellular consequences of TREM-1 activation, we have characterized global gene exp

28 The role for PGLYRP1 as a TREM-1 activator provides a new mechanism by which bacte

29 For the first time, these data show that TREM-1 aggravates inflammation in ALI by activating NLRP

30 Here we demonstrate for the first time that TREM-1 also plays an important role in transepithelial m

31 Hence, TREM-1 amplifies the inflammation induced by both bacter

32 TREM-1 amplifies Toll-like receptor-initiated responses

33 ering receptor expressed on myeloid cells 1 (TREM-1) amplifies inflammatory signaling.

34 onstitute a potent ligand capable of binding TREM-1 and inducing known TREM-1 functions.

35 ligands, targeted activation or blockade of TREM-1 and its ligands may help maximize the efficacy of

36 Levels of TREM-1 and of subpopulations of MVs were not different b

37 Structural similarity to TREM-1 and polymeric immunoglobulin receptor, and eviden

38 ering Receptor-1 Expressed on Myeloid cells (TREM-1) and Matrix MetalloPeptidase 9 (MMP-9) are detect

39 We showed that LR12, a TREM-1 antagonist peptide, significantly improved surviv

40 domain of TREM-1 (rTREM-1) and an agonistic TREM-1 antibody were used to inhibit and activate TREM-1

41 ering Receptor Expressed on Myeloid Cells-1 (TREM-1) are important effectors of the innate immune sys

42 We identified TREM-1 as a major upstream proatherogenic receptor.

43 profiling of hypoxic mature DCs and identify TREM-1 as a novel hypoxia-inducible gene that may amplif

44 TREM-1 associates with and signals via the adapter prote

45 exogenous administration of soluble forms of TREM-1 attenuates inflammation and markedly improves sur

46 1 activation, demonstrating that the PGLYRP1/TREM-1 axis can be activated in the absence of bacterial

47 permanent and transient myocardial ischemia, Trem-1 blockade also ameliorates cardiac function and li

48 Furthermore, TREM-1 blockade of ex vivo psoriatic DCs in an allogenei

49 lammatory myeloid DCs was developed to study TREM-1 blockade, and treatment with a TREM-1 blocking ch

50 study TREM-1 blockade, and treatment with a TREM-1 blocking chimera decreased allogeneic T-helper ty

51 Despite intense interest in soluble TREM-1, both as a clinical predictor of survival and as

52 These data imply direct activation of TREM-1 by filoviruses and also indicate that neutrophils

53 on of DAP12-deficient macrophages, whereas a TREM-1 chimera did not.

54 ere less inflammatory compared to plaques of Trem-1(+/+) chimeric mice.

55 trophils in vitro, and a soluble recombinant TREM-1 competitively inhibited the loss of cell surface

56 Therefore, targeting TREM-1 could be a novel therapeutic approach to enhance

57 These data suggest that TREM-1 could constitute a new therapeutic target during

58 on changes in human monocytes in response to TREM-1 cross-linking in comparison to and combined with

59 A peptide specific to TREM-1 diminished the release of tumor necrosis factor a

60 dendritic cells following activation through TREM-1, evidenced by higher expression of CD1a, CD86, an

61 roinflammatory myeloid cell surface receptor TREM-1 expressed by Kupffer cells is a crucial factor in

62 TREM-1, expressed by neutrophils and mature monocytes, i

63 he HIV-related proteins Tat or gp120 induces TREM-1 expression in macrophages and confers anti-apopto

64 After infarction, TREM-1 expression is upregulated in ischemic myocardium

65 TREM-1 expression was reduced with successful narrow ban

66 We report the crystal structure of the human TREM-1 extracellular domain at 1.47 A resolution.

67 We report the crystal structure of the mouse TREM-1 extracellular domain at 1.76A resolution.

68 ligand has hampered a full understanding of TREM-1 function.

69 capable of binding TREM-1 and inducing known TREM-1 functions.

70 We conclude that certain TLR and TREM-1 gene polymorphisms may be associated with CAD in

71 Concerning TREM-1 gene polymorphisms, we found that A/A genotype of

72 Trem-1 genetic invalidation or pharmacological inhibitio

73 ly supports the contention that the globular TREM-1 head is a monomer contrary to proposals of a symm

74 hether TGF-beta1 regulated the expression of TREM-1 in a mouse model of pulmonary fibrosis.

75 m-1(-/-) mice or pharmacological blockade of Trem-1 in ApoE(-/-) mice using LR-12 peptide also signif

76 Genetic invalidation of Trem-1 in ApoE(-/-)/Trem-1(-/-) mice or pharmacological

77 After genetically invalidating Trem-1 in chimeric Ldlr(-/-)Trem-1(-/-) mice and double

78 Engagement of TREM-1 in combination with microbial ligands that activa

79 Here, we investigated the potential role of TREM-1 in HIV latency in macrophages.

80 TGF-beta1 increased the expression of TREM-1 in mouse macrophages partly via the transcription

81 These data define a new function for TREM-1 in neutrophil migration across airway epithelial

82 encing identified that these proteins induce TREM-1 in p65-dependent manner.

83 ic patients, and there was increased soluble TREM-1 in the circulation of psoriasis patients.

84 t phases of the immune response, we examined TREM-1 in the context of host defense against microbial

85 We identified a critical role for Trem-1 in the upregulation of cluster of differentiation

86 Recent studies suggest a role for TREM-1 in viral immunity.

87 gering receptor expressed on myeloid cells-1(TREM-1) in orchestrating the inflammatory response that

88 ering receptor expressed on myeloid cells 1 (TREM-1) increases the expression of TGF-beta family gene

89 Activation through TREM-1 induces inflammatory cytokines, including IL-8, M

90 TREM-1 is a member of the Ig superfamily, active through

91 TREM-1 is a pivotal amplifier of the innate immune respo

92 her, our findings offer causal evidence that TREM-1 is a pivotal determinant of Kupffer cell activati

93 TREM-1 is a surface receptor implicated in innate and ad

94 TREM-1 is an amplifier of inflammatory response, and is

95 TREM-1 is the best-characterized member of a growing fam

96 gering receptor expressed on myeloid cells-1(TREM-1) is a member of the superimmunoglobulin receptor

97 ering receptor expressed on myeloid cells-1 (TREM-1) is critical for inflammatory signal amplificatio

98 ng human neutrophils, we identified a 15-kDa TREM-1 isoform in primary (azurophilic) and secondary (s

99 Thus, these data reveal that TREM-1 isoforms simultaneously activate and inhibit infl

100 Genetic invalidation of Trem-1 led to alteration of monocyte recruitment into at

101 r this activity through competition with the TREM-1 ligand.

102 The TREM-1 ligands are not known.

103 activating NLRP3 inflammasome, and blocking TREM-1 may be a potential therapeutic approach for ALI.

104 These novel data reveal that TREM-1 may play a critical role in establishing HIV rese

105 nes indicated that after WNV NY99 infection, TREM-1 mediated activation of toll-like receptors leads

106 ch, in turn, showed activity in blocking the TREM-1-mediated inflammatory responses in mice.

107 In conclusion, the TREM-1-mediated innate immune response played an essenti

108 In addition, TREM-1 mediates the septic shock pathway, and thus repre

109 lly invalidating Trem-1 in chimeric Ldlr(-/-)Trem-1(-/-) mice and double knockout ApoE(-/-)Trem-1(-/-

110 Genetic invalidation of Trem-1 in ApoE(-/-)/Trem-1(-/-) mice or pharmacological blockade of Trem-1 i

111 rem-1(-/-) mice and double knockout ApoE(-/-)Trem-1(-/-) mice, we pharmacologically inhibited Trem-1

112 This study aimed to determine the effect of TREM-1 modulation on LPS-induced ALI and activation of t

113 ibit inflammation via the canonical membrane TREM-1 molecule and this newly discovered granular isofo

114 TGF-beta1 increased expression of TREM-1 mRNA and protein in a time- and dose-dependent ma

115 Characterization of TREM-1 natural ligands will further illuminate the mecha

116 Here, we report that MARV and EBOV activate TREM-1 on human neutrophils, resulting in DAP12 phosphor

117 However, activation of TREM-1 on monocytes did drive robust production of proin

118 Our data suggest that activation of TREM-1 on monocytes participates during the early-induce

119 However, the effect of TREM-1 on NLRP3 inflammasome and ALI is still unknown.

120 Activation of TREM-1 on the GEC led to an increase in interleukin-8 (I

121 Where tested, positive TREM-1 outputs are greatly reduced by the PI3K inhibitor

122 including increased expression of the novel TREM-1 pathway and the IL-36 cytokine in patients with A

123 ggering receptor expressed on myeloid cells (TREM-1) plays a determinant role in macrophage atherogen

124 We have previously shown that TREM-1 prolongs survival of macrophages treated with lip

125 The addition of exogenous TREM-1sv inhibited TREM-1 receptor-mediated proinflammatory cytokine produc

126 Blockade of TREM-1 reduces inflammation and increases survival in an

127 Inhibition of TREM-1 reduces sepsis in mouse models, suggesting a role

128 erapeutic tool, the origin of native soluble TREM-1 remains controversial.

129 udy, the recombinant extracellular domain of TREM-1 (rTREM-1) and an agonistic TREM-1 antibody were u

130 rophils, resulting in DAP12 phosphorylation, TREM-1 shedding, mobilization of intracellular calcium,

131 , but certain genes such as CD36, CLEC4E, or TREM-1 showed human-specific expression.

132 tuted with bone marrow deficient for Trem-1 (Trem-1(-/-)) showed a strong reduction of atheroscleroti

133 Blockage of TREM-1 signaling caused a more severe proinflammatory re

134 The role of TREM-1 signaling in enhancement of the proinflammatory r

135 Blockage or activation of TREM-1 signaling lowered or raised the number of neutrop

136 Blockade of TREM-1 signaling may constitute an attractive novel and

137 Together, these data suggest that the TREM-1 signaling pathway may be a previously unidentifie

138 1 antibody were used to inhibit and activate TREM-1 signaling to evaluate its role in neutrophil acti

139 ering receptor expressed on myeloid cells 1 (TREM-1) signaling (eg, CCL2, CCL3, and single immunoglob

140 receptor expressed on myeloid cells type-1 (TREM-1) signaling was a major canonical pathway in the p

141 TREM-1 silencing in macrophages exposed to HIV-related p

142 TREM-1 stimulation activates neutrophils and monocytes a

143 The soluble form of TREM-1 (sTREM-1), a marker of TREM-1 activation, is dete

144 onomeric, consistent with our previous human TREM-1 structure, and strongly supports the contention t

145 etitively inhibited the loss of cell surface TREM-1 that otherwise occurred on neutrophils exposed to

146 ering receptor expressed on myeloid cells-1 (TREM-1), the natural killer cell-activating receptor NKp

147 TREM-1, the first to be identified, acts to amplify infl

148 reconstituted with bone marrow deficient for Trem-1 (Trem-1(-/-)) showed a strong reduction of athero

149 Da protein is a novel splice variant form of TREM-1 (TREM-1sv).

150 four of these, however, are direct homologs: TREM-1, TREM-2, TREM-like transcript 1 (TLT1), and TLT2.

151 biologic processes related to activation by TREM-1 (triggering receptor expressed on myeloid cells 1

152 Our previous study indicated that TREM-1 (triggering receptor expressed on myeloid cells 1

153 TREM-1 (triggering receptor expressed on myeloid cells),

154 TREM-1 (triggering receptor expressed on myeloid cells-1

155 -1(-/-) mice, we pharmacologically inhibited Trem-1 using LR12 peptide.

156 In psoriasis lesions, TREM-1 was colocalized with DCs, as well as CD31(+) endo

157 TREM-1 was expressed in human atherosclerotic lesions, m

158 We now show that TREM-1 was expressed in the skin of healthy and psoriati

159 In conclusion, we found the expression of TREM-1 was increased in lung tissues from mice with pulm

160 The expression of TGF-beta1 and TREM-1 was increased on day 7, 14, and 21 after single i

161 Expression of TREM-1 was up-regulated in response to TLR activation, a

162 ering receptor expressed on myeloid cells-1 (TREM-1) was upregulated 16-fold after 24 h of treatment

163 1H NMR spectroscopy of both human and mouse TREM-1, we have conclusively demonstrated the monomeric

164 of TLT-1, homologous to a fragment of murine TREM-1, which, in turn, showed activity in blocking the