ライフサイエンスコーパス: IP-10

1 ell migration toward chemokines (TARC/CCL17, IP-10).

2 of chemoattractants for monocytes (MCP-1 and IP-10).

3 (CXCL-10)/IFN-gamma-inducible 10-kD protein (IP-10).

4 ng beta 1 interferon (IFN-beta1) and CXCL10 (IP-10).

5 cal upregulation of TLR7-mediated cytokines (IP-10).

6 luding chemokines MIP-1alpha, MIP-1beta, and IP-10).

7 n FGF-Basic, IL-15, IL-6, IL-28A, ENA-78 and IP-10.

8 h low IP-10 had 64% SVR versus 24% with high IP-10.

9 (IL-1alpha, IL-8, IL-12(p70)) and increased IP-10.

10 GF, FGF-2, IL-8, TIMP-1, TIMP-2, GM-CSF, and IP-10.

11 reduced expression of iNOS, IL-6, MCP-1 and IP-10.

12 g the transendothelial migration response to IP-10.

13 class II and secretion of IL-8, RANTES, and IP-10.

14 th the "No Infect and No ACR" group (CXCL10 [IP-10]: 107.0 vs. 31.9 pg/mL [P=0.001] and IL-16: 472.1

15 high plasma levels of CXCL10 (also known as IP-10), a chemokine that directs T cells to sites of inf

16 ovel dialog between Ms and B cells, in which IP-10 acts as a PC differentiation factor.

17 comparable amounts of TNFalpha, IL-12p40 and IP-10 after infection with H3N2, in marked contrast to d

18 s (IL-6, CD163, IL-10, LBP, IL-2, MCP-1, and IP-10), all with ORs for the 3(rd) versus 1(st) tertile

19 Furthermore, IP-10 amplifies the production of IL-6 by B cells, which

20 ion with GRO-alpha (an agonist) but not with IP-10 (an inverse agonist).

21 ed alanine aminotransferase and pretreatment IP-10 and between the presence of cirrhosis and elevated

22 MACs might be mediated via downregulation of IP-10 and changes in ED:EI by MAC regulation of eNOS in

23 ines (IL-1beta, IL-12p70) were increased and IP-10 and elafin were decreased.

24 ined immunohistochemically for expression of IP-10 and eotaxin (n = 4 to 8/group).

25 In donor eyes, IP-10 and eotaxin expressions were increased in the RPE

26 that the relative balance between levels of IP-10 and eotaxin is critical in regulating the neovascu

27 IP-10 and eotaxin may be early biomarkers in AMD.

28 Both IP-10 and eotaxin were expressed by neovascular endothel

29 Both IP-10 and eotaxin were expressed in the neurosensory ret

30 nificantly lower dNK cell numbers and higher IP-10 and I-TAC levels versus gestational age-matched co

31 g a correlation with the IFN gene signature (IP-10 and I-TAC), and this score was compared between 26

32 ally enhanced mRNA and protein expression of IP-10 and I-TAC.

33 ocyte infiltration through the production of IP-10 and MCP-1.

34 We show that the CXCR3 chemokine ligands IP-10 and Mig (CXCL9) were highly induced in the brains

35 ynergy, production levels of CXCR3 cytokines IP-10 and MIG, depend non-linearly on both IFNgamma and

36 tes lung fibrosis by reducing lung levels of IP-10 and MIP-1alpha.

37 ession of the NF-kappaB-dependent chemokines IP-10 and MIP-1alpha.

38 On treatment, IP-10 and MIP-1beta levels were significantly higher in

39 gether contributing to the downregulation of IP-10 and other Th1 cell-recruiting chemokines (e.g., CX

40 Suppression of IP-10 and other Th1-biasing chemokines by P. gingivalis

41 The combination of serum level of IP-10 and SNPs in IL28B can identify patients with AHC w

42 sfusion need; IL-2R, IL-8, and leukocytosis; IP-10 and thrombocytopenia; HGF, MIG, IL-1RA, and marked

43 ) and plasmacytoid DCs (pDCs), production of IP-10 and type-I IFN, and expression of type-I IFN-relat

44 CD138(+)CD38(++) PCs through secreted CXCL10/IP-10 and VCAM-1 contact.

45 rrelation was seen between PGE(2) levels and IP-10 and VEGF (P = 0.04).

46 nes, including GM-CSF, IFN-alpha2, IL-12p70, IP-10 and VEGF, during both acute and chronic stages of

47 ive diabetic retinopathy, and correlate with IP-10 and VEGF.

48 to determine the association between CXCL10 (IP-10) and ACR in LTRs.

49 t association was found only between CXCL10 (IP-10) and ACR.

50 and inhibition of IFN-gamma-induced CXCL10 (IP-10) and FcgammaRI (CD64) indicated that inhibition by

51 The levels of both CXCL10 (IP-10) and IL-16 were significantly increased in histolo

52 ng levels of IFN-gamma-inducible protein-10 (IP-10) and MIP-1alpha.

53 at therapeutic strategies to inhibit CXCL10 (IP-10) and or its cognate receptor, CXCR3, warrant inves

54 er levels of IFN-gamma-inducible protein-10 (IP-10) and tumor necrosis factor-related apoptosis-induc

55 We measured CXCL10 (IP-10) (and other cytokines previously implicated in the

56 reased CSF levels of CCL3, CCL5, and CXCL10 (IP-10), and decreased activation of both resident CNS an

57 kin 10, interferon gamma-induced protein 10 (IP-10), and hepatocyte growth factor differentiated betw

58 otein-1, interferon-gamma-inducible protein (IP-10), and macrophage inflammatory protein-1delta) were

59 CCL4 (MIP-1beta), CCL5 (RANTES), and CXCL10 (IP-10), and promoting chemotaxis of macrophages and CD4(

60 M-1), interferon-gamma-inducible protein 10 (IP-10), and the signaling intermediates Janus kinase 1,

61 induced massive upregulation of MIP-1alpha, IP-10, and IFN-alpha in normal blood mononuclear cells.

62 lular parasite, induced production of CXCL9, IP-10, and IL-6 in LC.

63 nflammatory protein (MIP)-1alpha, MIP-1beta, IP-10, and interleukin-6.

64 and the radioresistant cells most of the KC, IP-10, and MCP-1 cytokines.

65 nchial epithelial cells induces apical IL-8, IP-10, and MCP-1 secretion independent of infection, sug

66 ed in infected A1-KO mice, but levels of KC, IP-10, and MCP-1 were increased.

67 ely to have higher peak levels of IFN-gamma, IP-10, and MIG after vaccination than were revaccinated

68 ines and chemokines, including IL-6, RANTES, IP-10, and MIP-3a, which were regulated by NFkappaB sign

69 (growth-related oncogene alpha [GRO-alpha], IP-10, and monokine induced by gamma interferon [MIG]),

70 howed significantly higher levels of IL-17A, IP-10, and RANTES in the lung.

71 on) protein elicited the production of IL-8, IP-10, and RANTES.

72 IS (not on CTC) IL-6, IL-8, IL-12p40, IL-18, IP-10, and TNF increased during 2 weeks (P </= .04) of A

73 a], 10-kDa gamma interferon-induced protein [IP-10]) and proinflammatory (interleukin 1 receptor anta

74 n [IL]-6, IL-8, IL-15, IL-16, IL-17, CXCL10 [IP-10], and MCP-1 [CCL2]) in BAL samples (n=233) from pa

75 ls of interferon-gamma-inducible protein-10 (IP-10) are predictive of treatment-induced clearance in

76 clampsia compared with controls, identifying IP-10 as a novel, robust early predictor of preeclampsia

77 letokine expression in beta-cells and reveal IP-10 as a primary therapeutic target to prevent beta-ce

78 ther studies should evaluate the benefits of IP-10 as a triage approach to monitor ART in resource-li

79 more likely to have a measurable decline in IP-10 at day 7 than clinically diagnosed cases (48/77 (6

80 Logistic regression was used to build an IP-10-based model able to identify individuals with VL >

81 ficantly higher levels of interleukin 18 and IP-10 but lower levels of hepatocyte growth factor than

82 expressed by basal keratinocytes and CXCL10/IP-10 by keratinocytes and endothelial cells during woun

83 Full induction of IP-10 by MRP8/MRP14 required synergy between the transcr

84 tes/macrophages, and found that induction of IP-10 by MRP8/MRP14 required Toll-like receptor 4 and TR

85 presence of S. aureus The downregulation of IP-10 by S. aureus was mediated by components of its cel

86 ions and the proinflammatory mediators IL-6, IP-10, CCL2, and CCL3.

87 uction in the serum concentration of CXCL10 (IP-10), CCL22 (MDC), CCL17 (TARC), CCL-2 (MCP-1) and CCL

88 nasal aspirate IFN-gamma, CXCL8/IL-8, CXCL10/IP-10, CCL5/RANTES, CCL11/eotaxin-1, CCL2/MCP-1, CCL4/MI

89 nes and receptors (IL-22, CCL27, MIP-1alpha, IP-10, CCR4, CCR5, and CXCR3), immune dysfunctional rece

90 Ai also down-regulated the production of the IP-10 chemokine in HIV-infected human microglia.

91 ctively), whereas ratios of IFN-gamma-evoked IP-10 chemokine were low in all groups.

92 nterferon-inducible cytokines OAS and CXCL10/IP-10 compared with control mice treated with fluticason

93 The peak of serum IP-10 concentration was at intermediate dry AMD.

94 rmed that donor islet-specific expression of IP-10 contributed to islet inflammation and loss of beta

95 The effects of islet-derived IP-10 could be blocked by treatment of donor islets and

96 erved in stromal cell-derived factor-1alpha, IP-10, cutaneous T-cell-attracting chemokine, monokine i

97 ed levels of IFN-gamma-inducible protein 10 (IP-10/CXCL), IL-8, and MCP-1, all of which have been rep

98 f interleukin 12, IFN-gamma, and chemokines (IP-10/CXCL-10, MCP-1/CCL-2, MIP-1alpha/CCL-3, RANTES/CCL

99 nduce the expression of the T-cell chemokine IP-10 (CXCL10) from neutrophils, peripheral blood mononu

100 and the IFN-inducible CXCR3 chemokine ligand IP-10 (CXCL10) was recently found to be the only serum b

101 ecombinant RABVs expressing RANTES (CCL5) or IP-10 (CXCL10).

102 IFN-gamma-induced protein of 10-kDa (IP-10)/CXCL10 and macrophage-derived chemokine (MDC)/CCL

103 he chemokine IFN-gamma inducible protein 10 (IP-10)/CXCL10.

104 1alpha (CCL3), and IFN inducible protein-10 (IP-10, CXCL10) were also elevated.

105 .001), IL-6 (P<0.001), IL-8/CXCL8 (P<0.001), IP-10/CXCL10 (P<0.05), MCP-1/CCL2 (P<0.05), macrophage i

106 All patients showed a prompt clinical and IP-10/CXCL10 response.

107 eficial for treatment of PFAPA attacks, with IP-10/CXCL10 serving as a potential biomarker.

108 1RN, CASP1, IL18RAP), and IFN-induced (AIM2, IP-10/CXCL10) genes were significantly overexpressed, bu

109 ytokine interferon-gamma-induced protein 10 (IP-10/CXCL10) was among the highest released, and high l

110 okine targets in skeletal muscle (IL-1ra and IP-10/CXCL10) were identified from a cytokine array.

111 le chemokines IFNgamma-inducible protein 10 (IP-10/CXCL10), IFN-inducible T cell alpha chemoattractan

112 eron-gamma (IFN-gamma)-inducible protein 10 (IP-10/CXCL10), monokine induced by IFN-gamma (Mig/CXCL9)

113 Especially IL-6, but also IP-10/CXCL10, and VEGF may be interesting mediators in R

114 NA encoding TSLP, TARC/CCL17, MDC/CCL22, and IP-10/CXCL10, but not I-TAC/CXCL11 and I-309/CCL1, were

115 MDC/CCL22, I-309/CCL1), and Th1-attracting (IP-10/CXCL10, I-TAC/CXCL11) chemokines in the bronchial

116 y affected by GSK3beta inactivation included IP-10/CXCL10, MCP-1/CCL2, IL-8/CXCL8, RANTES/CCL5, and G

117 s of chemokines for activated T lymphocytes (IP-10/CXCL10, MIG/CXCL9), G-CSF, and proinflammatory cyt

118 nt ELR-devoid CXC chemokines (ie, PF4/CXCL4, IP-10/CXCL10, MIG/CXCL9, and IP-9/CXCL11), we sought to

119 ophage inflammatory protein 2 (MIP-2)/CXCL2, IP-10/CXCL10, MIP-1alpha/CCL3, granulocyte colony-stimul

120 ated negatively with serum concentrations of IP-10/CXCL10, whereas CD4(+)/HLA-DR(+) T lymphocyte coun

121 lloproteinase 9 (1.30), the interaction term IP-10/CXCL10xwomen (0.69), and the interaction term thro

122 teins CD3, CD4, CD8, CTLA4, Foxp3, chemokine IP-10, cytotoxic perforin and granzyme B, and BKV VP1 mR

123 IP-10-deficient and WT animals had comparable acute infa

124 IP-10-deficient mice challenged with NP-Ficoll show a de

125 IP-10 did not modulate cardiac fibroblast proliferation

126 ost participants had a measurable decline in IP-10 during the first 7 days of therapy.

127 In addition, IP-10 enhanced growth factor-mediated wound contraction

128 PK) activity, which differentially regulated IP-10 expression and subsequent protein release.

129 Calcitriol reduced IP-10 expression by MACs (p<0.0006), and blockade of IP-

130 ed a novel signaling mechanism that controls IP-10 expression in monocytes/macrophages by MRP8/MRP14,

131 IP-10 expression was inhibited in a dose-dependent manne

132 The chemokine CXCL10/IP-10 facilitates recruitment of Th1-type leukocytes to

133 -gamma), and IFN-gamma-inducible protein 10 (IP-10) from the arrays for further investigation and ass

134 and p300 histone acetyltransferase with the IP-10 gene required p38 and c-Jun N-terminal kinase mito

135 In vitro studies showed induction of the IP-10 gene was mediated by calcineurin-dependent NFAT si

136 ma (GM, 5.44 vs 23.41 pg/ml; p = 0.009), and IP-10 (GM, 29.43 vs 281.7 pg/ml; p = 0.007) responses fo

137 , IL-6; Interferon-gamma-induced Protein 10, IP-10; Granulocyte-stimulating factor, G-CSF) in the med

138 Using a cutoff value of IP-10 >/=44.2 pg/mL, the model identified detectable VL

139 CT carriers with low IP-10 had 64% SVR versus 24% with high IP-10.

140 interferon [IFN] gamma-inducible protein 10 [IP-10]) have been associated with hepatic fibrosis in pr

141 Infarcted IP-10(-/-) hearts exhibited accentuated early dilation,

142 taining of first trimester decidua localized IP-10, I-TAC, IFN-gammaR1, and -R2 to vimentin-positive

143 CCL11 (Eotaxin-1), CXCL1 (GROalpha), CXCL10 (IP-10), IFN-gamma, IL-4, IL-5, IL-7, IL-12p70, IL-13, IL

144 mokines and cytokines CCL5 (RANTES), CXCL10 (IP-10), IL-1alpha, IL-1beta, and PGE(2), which have prev

145 Four additional analytes (IP-10, IL-12/23p40, IFNy, IL-15) were found to be elevat

146 Statistical analysis showed that IP-10, IL-6, IL-17, and IL-2 were increased in H7N9 infe

147 ed circulating MCP-1, TNFalpha, IFNgamma and IP-10 in blood.

148 ntial role for proinflammatory mediators and IP-10 in combination with the vaginal-health-score as pr

149 he mechanisms by which MRP8/MRP14 stimulates IP-10 in monocytes/macrophages, and found that induction

150 (+) cells was dependent on the production of IP-10 in monocytes/macrophages.

151 locyte colony-stimulating factor (G-CSF) and IP-10 in nasal wash.

152 sed expression of the T cell chemoattractant IP-10 in sciatic nerves.

153 d supports the notion of a potential role of IP-10 in the immunopathogenesis of RA.

154 Higher values of CXCL10 (IP-10) in BAL fluid are associated with ACR in LTRs, sug

155 CXCL10 (interferon gamma-induced protein 10, IP-10) increase in plasma and the peritoneal cavity afte

156 In contrast, overexpression of RANTES or IP-10 increased RABV pathogenicity by causing neurologic

157 fractalkine distinguish TCR-induced TEM from IP-10-induced TEM.

158 IP-10(-/-) infarcts had more intense infiltration with C

159 is and epithelial cells was not required for IP-10 inhibition.

160 K but weak JNK activation, resulting in high IP-10 (interferon-inducible protein 10), tumor necrosis

161 nic (TNFalpha [tumor necrosis factor alpha], IP-10 [interferon gamma-induced protein 10]), and proinf

162 P-2), interferon gamma inducible protein-10 (IP-10), interferon gamma (IFN-gamma), tumor necrosis fac

163 feron (IFN)-gamma, IFN-inducible protein-10 (IP-10), interleukin (IL)-6, and tissue inhibitor of meta

164 nvaccinated individuals, induced protein 10 (IP-10), interleukin 10 (IL-10), macrophage inflammatory

165 (VEGF), interferon gamma-induced protein 10 (IP-10), interleukin-8 (IL-8), epidermal growth factor (E

166 IP-10 is an accurate biomarker to screen individuals on

167 Endogenous IP-10 is an essential inhibitory signal that regulates t

168 IP-10 levels mirror HCV RNA, suggesting that IP-10 is an indicator of innate immune viral recognition

169 The receptor for IP-10 is CXCR3, and MRP8/MRP14-induced chemotaxis of CXC

170 CXCL10 (IP-10) is a potent chemoattractant for T cells that has

171 as interferon-gamma-inducible 10-kd protein [IP-10]) is a chemokine that potentially plays a role in

172 interferon (IFN-gamma)-stimulated release of IP-10, ITAC (CXCL11), and Mig (CXCL9) from epithelial ce

173 eatment blindly using a previously described IP-10 kinetic algorithm.

174 for previously described TB markers, such as IP-10, LBP, FCG3B, and TSP4, and for many novel proteins

175 an IP-10 level <540 pg/mL and 32% who had an IP-10 level >540 pg/mL) (P < .01).

176 ontaneous clearance (83% of those who had an IP-10 level <540 pg/mL and 32% who had an IP-10 level >5

177 An increased baseline IP-10 level was associated with a T allele in the IL28B

178 lysis, factors independently associated with IP-10 levels >/=150 pg/mL (median level) included HCV RN

179 of 165) and in those with and without plasma IP-10 levels >/=380 pg/mL.

180 hereas the negative predictive value of high IP-10 levels (>600 pg/mL) was 67%.

181 The positive predictive value of low IP-10 levels (<600 pg/mL) for SVR was 69%, whereas the n

182 Here we investigate the early response in IP-10 levels (between day 0 and day 7 of TB therapy) to

183 te HCV detection and the association between IP-10 levels and spontaneous clearance were assessed in

184 High IP-10 levels at acute HCV detection were associated with

185 onfirmed cases were more likely to have high IP-10 levels at D0 and had a steeper decline than clinic

186 resent study, factors associated with plasma IP-10 levels at the time of acute HCV detection and the

187 earance had significantly higher mean plasma IP-10 levels at the time of acute HCV detection than tho

188 nfirms the association between a decrease in IP-10 levels during the first week of treatment and a ba

189 Significantly elevated IP-10 levels in first trimester sera from women eventual

190 Circulating IP-10 levels in human blunt trauma patients were correla

191 We evaluated IP-10 levels in pretreatment serum from 115 nonresponder

192 ), whereas during week 2 the mean decline in IP-10 levels in treatment-naive patients (-14%) was sign

193 Including data on IP-10 levels increased the ability of the IL28B rs129798

194 Changes in IP-10 levels mirror HCV RNA, suggesting that IP-10 is an

195 At week 1, the mean decline in plasma IP-10 levels was the same in treatment-naive and treatme

196 IL28B genotype and baseline IP-10 levels were additive but independent when predicti

197 Lower plasma IP-10 levels were associated with spontaneous clearance

198 Serum eotaxin and IP-10 levels were significantly elevated in all stages o

199 IP-10 levels were significantly higher in subjects with

200 We assessed the combination of pretreatment IP-10 levels with IL28B genotype as predictors of treatm

201 Serum IP-10 levels within the IL28B genotype groups provided a

202 Patients with acute HCV and high baseline IP-10 levels, particularly >380 pg/mL, should be conside

203 7) and interleukin (IL)-5 and an increase in IP-10 levels.

204 Plasma interferon-gamma-induced protein 10 (IP-10) levels declined significantly upon dosing with RG

205 easured interferon gamma-induced protein 10 (IP-10) levels in 428 patients at baseline, week 1, and w

206 on of interferon-gamma-inducible protein-10 (IP-10) may also differentiate antiviral response.

207 ted in reduced milk levels of the chemokines IP-10, MCP-1, MCP-3, MCP-5 and MIP-1beta, which in turn

208 Mean IP-10, MCP-1, MIP-1beta, and IL-18 levels all decline on

209 genotype is combined with pretreatment serum IP-10 measurement, the predictive value for discriminati

210 IP-10-mediated actions may be due, at least in part, to

211 IL-17 and the lymphocyte chemokines IP-10, MIG, MIP-1alpha, MIP-1beta, and RANTES were decre

212 and marked splenomegaly; and IL-1RA, IL-2R, IP-10, MIP-1beta, and JAK2V617F.

213 with SM produced significantly higher IL-10, IP-10, MIP-1betam and MCP-2.

214 f MDX-1100, a fully human, anti-CXCL10 (anti-IP-10) monoclonal antibody, in RA patients whose disease

215 ma levels of IFN-gamma-inducible protein 10 (IP-10), monocyte chemoattractant protein 1 (MCP-1), macr

216 nterferon-gamma-inducible protein of 10 kDa (IP-10), monocyte chemoattractant protein-1 (MCP-1), tumo

217 n 8 (IL-8), interferon-inducible protein 10 (IP-10), monocyte chemotactic protein 1 (MCP-1), and RANT

218 IL-8, interferon-gamma inducible protein-10 [IP-10], monocyte chemoattractant protein-1, macrophage i

219 actor (HGF), IFN-gamma-inducible protein 10 (IP-10), monokine induced by IFN-gamma (MIG), monocyte ch

220 A-normalized measures of CD3epsilon mRNA and IP-10 mRNA and 18S rRNA that is diagnostic and predictiv

221 A molecular signature of CD3epsilon mRNA, IP-10 mRNA, and 18S rRNA levels in urinary cells appears

222 of IL28B and IFN-gamma-inducible protein 10 (IP-10) mRNA relies on TT/-G, but not rs12979860, making

223 on mRNA and interferon-inducible protein 10 (IP-10) mRNA, and 18S rRNA discriminated between biopsy s

224 Anti-IL-6, -FGF, or -CXCL-10/IP-10 neutralizing antibodies ablated the protective eff

225 of donor islets and recipient mice with anti-IP-10 neutralizing monoclonal antibody.

226 METHODS AND We studied cardiac repair in IP-10-null and wild-type (WT) mice undergoing reperfused

227 Although IP-10-null and WT mice had comparable cytokine expressio

228 rction protocols and examined the effects of IP-10 on cardiac fibroblast function.

229 CXCR3 ligands, CXCL11/IP-9/I-TAC and CXCL10/IP-10, on the EGF- and VEGF-induced redistribution of m-

230 high level of interferon-induced protein 10 (IP-10 or CXCL10) and hepatitis B surface and e antigens

231 Incubation of pNK cells with either IP-10 or I-TAC elicited concentration-dependent enhanced

232 Mice deficient in IP-10 or Mig were both partially protected against cereb

233 Genetically deleting either Ip-10 or Mip-1alpha in Mmp-8(-/-) mice abrogates their l

234 down-regulated MalAg-specific IFN-gamma and IP-10 (p < 0.001) responses in Fil(+).

235 P < .001), IL-8 (P < .001), IL-10 (P = .01), IP-10 (P = .0001), MDC (P < .001), MIP-1alpha, (P < .001

236 Higher plasma levels of IP-10 (P = .0011), TNF-RII (P = .0002), and D-dimer (P =

237 01), IL-12 (P < .001), IL-15 (P = .001), and IP-10 (P = .003) were independently predictive of inferi

238 ), IL-6 (P = 0.0396), IL-8 (P = 0.0169), and IP-10 (P = 0.0045) secretion during in vitro stimulation

239 LTNP-C showed lower plasma IP-10 (p=0.019) and higher IFN-gamma (p=0.02) levels tha

240 a and suggest that the CXCR3 ligands Mig and IP-10 play distinct, nonredundant roles in the pathogene

241 ls of interferon gamma inducible protein 10 (IP-10) predict outcomes of antiviral therapy in patients

242 IP-10 production by Ms is induced by B cell-derived IL-6

243 n increased gamma interferon (IFN-gamma) and IP-10 production within the septic peritoneum together w

244 lower IL-6 release while maintaining higher IP-10 production, skewing toward the type I interferon p

245 activation of NF-kappaB and IRF3 as well as IP-10 production.

246 no NELF or polymerase is detectible near the IP-10 promoter before induction, and LPS-dependent polym

247 n 6 (IL-6), interferon-inducible protein 10 (IP-10), RANTES, and IL-1beta.

248 Poly(I-C)-induced expression of IP-10, RANTES, and IFN-beta mRNA was decreased in MKK4-

249 phage inflammatory protein 1alpha/CCL-3, and IP-10), reactive oxygen species (ROS), and nitric oxide,

250 alpha-SMA(+) cells that expressed CXCR3, the IP-10 receptor.

251 ed vFLIP-induced expression of the chemokine IP-10, reduced vFLIP-induced cell proliferation and incr

252 relieved P. gingivalis-induced inhibition of IP-10 release.

253 nd IFN-gamma-inducible protein 10 (CXCL10 or IP-10) remained statistically significant in the multiva

254 es (TNFalpha) within minutes whereas others (IP-10) require hours remains unclear.

255 L-6 and interferon gamma-induced protein 10 (IP-10) respectively.

256 and reduced IFN-gamma-inducible protein 10 (IP-10) response to TLR2 stimulation (P = .042).

257 d individuals had earlier peaks in IL-10 and IP-10 responses that occurred at much lower viral loads

258 pression by MACs (p<0.0006), and blockade of IP-10 restored the angiogenic capacity of MACs from pati

259 However, the absence of IP-10 resulted in a hypercellular early reparative respo

260 (CXCL9) from epithelial cells and inhibited IP-10 secretion in a mixed infection with the otherwise

261 expression and suppressed rhinovirus-induced IP-10 secretion, which was associated with increased vir

262 UA and OA (25 muM) reduced the synthesis of IP-10; sICAM-1, IL-23 and GROalpha were slightly repress

263 Of 70 markers, CXCL10 (IP-10), sIL-1RII, sIL-2RA, and CCL3 (MIP-1A) were strong

264 d Mig staining of endothelial cells, whereas IP-10 staining was mainly found in neurons.

265 s was associated with the release of CXCL10 (IP-10), suggesting that this adjuvant formulation may ha

266 uced the release of IL-6, IL-8, TNFalpha and IP-10, suggesting that NS1 protein of Udorn does not (ef

267 DL-C and reductions in HIV RNA level, MCP-1, IP-10, sVCAM-1, sTNFR2, and sCD14.

268 TNF, macrophage infiltration, and release of IP-10 that was induced with anti-CTLA-4 mAb.

269 of Th1 cell-recruiting chemokines, including IP-10, through an IFN-gamma-dependent mechanism.

270 IP-10 thus may be a surrogate marker of the rate of intr

271 perating characteristic analyses showed that IP-10, TNF-alpha, and IL-2 responses achieved high sensi

272 with siRNA directed against TNF-alpha, KC or IP-10 to mice suffering from dextran sulfate sodium (DSS

273 IFN-alpha, IFN-beta, IFN-gamma, IFN-lambda1, IP-10, TRAIL), cell recruiting (G-CSF, IL-1beta, IL-8, M

274 for TT and CC carriers with low versus high IP-10 (TT, 48% versus 20%; CC, 89% versus 79%).

275 IFN-gamma, interferon-inducible protein-10 (IP-10), tumor necrosis factor (TNF)-alpha, IL-1ra, IL-2,

276 CTC had lower interferon gamma (IFN-gamma), IP-10, tumor necrosis factor (TNF), interleukin (IL)-6,

277 IP-10 univariate model demonstrated high classification

278 on-associated marker genes (TNF-alpha, IL-8, IP-10) using qRT-PCR.

279 IP-10 was abundant in the connective tissue matrix assoc

280 mparable cytokine expression, the absence of IP-10 was associated with marked alterations in the cell

281 The median level of IP-10 was lower among patients with AHC and spontaneous

282 Mean IP-10 was lower in sustained responders compared with no

283 laminar deposits in all stages of AMD, while IP-10 was mainly in eyes with GA and CNV.

284 Moreover, the IFN-dependent chemokine IP-10 was produced in substantial amounts by pDCs in res

285 operating characteristic analysis, 540 pg/mL IP-10 was set as the cutoff for patients most likely to

286 ent on CXCR3 signaling, and the CXCR3 ligand IP-10 was sufficient to recruit monocytes to the adventi

287 A one-log increase of CXCL10 (IP-10) was associated with a 40% higher risk of ACR (odd

288 n addition, interferon-inducible protein 10 (IP-10) was identified as playing an important role in Ni

289 e Th1-associated chemokines RANTES, MIG, and IP-10 were each elevated significantly in the livers of

290 ory protein 1alpha (MIP-1alpha), RANTES, and IP-10 were individually cloned into the genome of attenu

291 rase chain reaction; serum concentrations of IP-10 were measured by enzyme-linked immunosorbent assay

292 Dose-related increases in nasal and serum IP-10 were observed 24 hours after doses 1 and 8 (>95% c

293 te chemoattractant protein 1, TNF-alpha, and IP-10 were observed in ZIKV-infected pregnant women carr

294 e transcripts for TLR7, RelA, IFN-gamma, and IP-10 were significantly downregulated between 2- and 3-

295 Furthermore, IL-6 and the chemokine IP-10 were significantly higher in severe H7N9 patients

296 nocyte chemoattractant protein 1[MCP-1], and IP-10) were increased.

297 Nasal and serum IFN-inducible protein 10 (IP-10) were measured after doses 1 and 8, then 1 (follow

298 ls of interferon-gamma-inducible protein 10 (IP-10) were quantified by enzyme-linked immunosorbent as

299 Finally, we demonstrated that the chemokine IP-10, which is induced by IFN-alpha and VRP-GFP, is dir

300 60 and rs8099917, along with serum levels of IP-10, with outcomes of patients with acute hepatitis C