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 ve a significant effect in the expression of TREM-1 and inflammatory mediators.

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

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

38 TREM-1 and PGLYRP1 levels were analyzed by ELISA.

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

40 Both the TREM-1 and the aMMP-8 (IFMA) levels were significantly e

41 ering receptor expressed on myeloid cells-1 (TREM-1) and its putative ligand the neutrophil peptidogl

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

43 ering receptor expressed on myeloid cells-1 (TREM-1) and the ICAM-1(+) neutrophils involve Rho GTPase

44 on and molecular pathways that link low ESS, TREM-1, and inflammation using a sophisticated in-vitro

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

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

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

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

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

50 ering receptor expressed on myeloid cells-1 (TREM-1) as well as increased CXCL1 and CXCL10 secretion.

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

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

53 1 activation, demonstrating that the PGLYRP1/TREM-1 axis can be activated in the absence of bacterial

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

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

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

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

58 ency of ICAM-1(+) BMDN, while rmCIRP-treated TREM-1(-/-) BMDN or pretreatment of BMDN with TREM-1 inh

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

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

61 wed that low ESS increased the expression of TREM-1 by the cultured cells leading to increased produc

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

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

64 id cells/cold inducible RNA binding protein (TREM 1/CIRP) ligand/receptor.

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

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

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

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

69 ivation markers CD80 and CD86 by UVB-induced TREM-1+ DCs.

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

71 ering receptor expressed on myeloid cells 1 (TREM-1) drives inflammatory responses in several cardiov

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

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

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

75 AngII infusion stimulated TREM-1 expression and activation on Ly6Chi monocytes thr

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

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

78 gnaling on peripheral monocytes and TLR2 and TREM-1 expression on NK cells.

79 TREM-1 expression was detected in mouse aortic aneurysm

80 TREM-1 expression was reduced with successful narrow ban

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

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

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

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

85 iption factors that appear to upregulate the TREM-1 gene expression in response to low ESS.

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

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

88 Trem-1 genetic invalidation or pharmacological inhibitio

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

90 strong positive correlations with levels of TREM-1, IL-1beta and MMP-8.

91 Our objective was to explore the role of TREM-1 in a mouse model of angiotensin II-induced (AngII

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

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

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

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

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

97 Depletion of TREM-1 in EV-A71-infected PBMCs with peptide LP17 result

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

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

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

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

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

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

104 uman cells, and the potential involvement of TREM-1 in the severe disease pathogenesis, thus providin

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

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

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

108 ering receptor expressed on myeloid cells-1 (TREM-1) in the mechanotransduction signaling pathways th

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

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

111 REM-1(-/-) BMDN or pretreatment of BMDN with TREM-1 inhibitor LP17 significantly decreased the freque

112 re warranted to investigate the potential of TREM-1 inhibitors as adjunctive anti-atherosclerotic the

113 ering receptor expressed on myeloid cells 1 (TREM-1), interleukin-1 beta (IL-1beta) were analyzed by

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

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

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

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

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

119 In conclusion, TREM-1 is involved in AAA pathophysiology and may repres

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

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

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

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

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

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

126 t had a negative aMMP-8 PoC test result, and TREM-1 levels < 75 pg/mL (P < 0.05).

127 evated aMMP-8 levels) together with elevated TREM-1 levels had a significantly higher number of perio

128 MA showed a strong positive correlation with TREM-1 levels in saliva (r = 0.777, P < 0.001).

129 ents showed higher salivary PGLYRP1, but not TREM-1 levels.

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

131 The TREM-1 ligands are not known.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

150 ering receptor expressed on myeloid cells 1 (TREM-1) on monocytes, NK, and NK-T cells was measured.

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

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

153 ering receptor expressed on myeloid cells 1 (TREM-1), peptidoglycan recognition protein 1 (PGLYRP1),

154 TREM-1, PGLYRP1, and IL-1beta could not distinguish betw

155 Salivary TREM-1, PGLYRP1, IL-1beta, and calprotectin were analyze

156 gene deletion (Apoe-/-Trem1-/-), as well as TREM-1 pharmacological blockade with LR-12 peptide, limi

157 TREM-1 plays a critical role in the eCIRP-mediated incre

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

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

160 ciated with (1) upregulation of TLR2 and (2) TREM-1 receptor expression on NK.

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

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

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

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

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

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

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

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

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

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

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

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

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

174 1 antibody were used to inhibit and activate TREM-1 signaling to evaluate its role in neutrophil acti

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

176 ering receptor expressed on myeloid cells-1 (TREM-1) signaling in classically activated macrophages a

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

178 ering receptor expressed on myeloid cells 1 (TREM-1) signalling.

179 Mechanistically, blocking TREM-1 significantly increased the expression level of t

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

181 TREM-1 stimulation activates neutrophils and monocytes a

182 Conversely, antibody-mediated TREM-1 stimulation exacerbated Ly6Chi monocyte aorta inf

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

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

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

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

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

188 n, our studies have identified a UVB-induced TREM-1+ tolerogenic DC subset and demonstrated an import

189 Further studies defined a TREM-1+ tolerogenic DC subset in the draining lymph node

190 Furthermore, TREM-1 transcriptional inhibition with siRNA in endothel

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

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

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

194 is study found that the signaling pathway of TREM-1 (triggering receptor expressed on myeloid cells 1

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

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

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

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

199 -1(-/-) mice, we pharmacologically inhibited Trem-1 using LR12 peptide.

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

201 In human AAA, TREM-1 was detected and TREM1 mRNA expression correlated

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

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

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

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

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

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

208 1H NMR spectroscopy of both human and mouse TREM-1, we have conclusively demonstrated the monomeric

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

210 Blocking TREM-1 with an antagonistic peptide LP-17 significantly