ライフサイエンスコーパス: monokine

1 ligands than human interferon-gamma-induced monokine.

2 nuclear factor kappaB (NF-kappaB)-dependent monokines.

3 erent costimulatory signals from these three monokines.

4 on of the production of many proinflammatory monokines.

5 volved in regulating IFN-gamma production by monokine-activated NK cells are not clearly identified.

6 Further, supernatants of monokine-activated NK cells obtained from both normal do

7 s by autologous NK cells and, hence, renders monokine-activated NK cells susceptible to NKp80-mediate

8 Hlx expression is induced in monokine-activated NK cells, but with delayed kinetics c

9 Here, we demonstrate that monokine-activated NK cells, isolated from both normal a

10 egative regulator of IFN-gamma production in monokine-activated NK cells.

11 Following trauma, increased inflammatory monokine activation and depressed APC function can occur

12 normal donors and subjected them to a novel monokine activation culture scheme.

13 of SHIP1 in CD56bright NK cells followed by monokine activation substantially lowered IFN-gamma prod

14 an important role in vivo in down-regulating monokine and IFN-gamma responses to acute intracellular

15 disruption suppressed IFN-gamma induction in monokine and/or CD16-stimulated NK cells.

16 -deficient mice, despite local expression of monokines and IFN-gamma.

17 protein-10 (IP-10), interferon-gamma-induced monokine, and interferon-inducible T cell alpha-chemoatt

18 in isolated human NK cells, proinflammatory monokines antagonize antiinflammatory TGF-beta signaling

19 preferentially targeted NF-kappaB-regulated monokines, ASA acted predominantly by suppressing IFNgam

20 Exposure of NK cells to monokines associated with conversion into memorylike cel

21 en) can trigger the expression of these four monokines by murine inflammatory macrophages.

22 The monokine combination IL-12, IL-18, and IFN-alpha substit

23 cing high levels of IFN-gamma in response to monokine costimulation.

24 Whereas CSA activates monocytes (to secrete monokines), CSB activates B-cells (to proliferate).

25 ll proliferation and watershed production of monokines (e.g. tumor necrosis factor alpha, interleukin

26 IL-12 and IL-18, but not other monokines, elicited secretion of IFN-gamma and IFN-gamma

27 n the levels of FcgammaRs, HLA antigens, and monokines, elutriated HMOs and U937 cells were transfect

28 AICL on monokine-exposed NK cells elicits NKp80-dependent effect

29 for neutralized IL-1 alpha, suggesting the 2 monokines have separate roles in promoting IgG2.

30 protein (IP-10) and IFN-gamma- induced human monokine (HuMig), but with a significantly higher affini

31 Monokines (i.e., interleukin [IL]-12, -18, and -15) indu

32 For example, the monokine IL-15 appears to be required for type 2 cytokin

33 We demonstrate that when activated by the monokines IL-12, IL-15, and IL-18, these NK cells promot

34 ytes with SAA stimulated the proinflammatory monokines IL-6 and IL-1beta concurrently with the M2 mar

35 Addition of NK cells that were activated by monokines (IL-12, IL-15, and IL-18) or by exposure to M.

36 Here we compared the effects of three monokines (IL-18, IL-15, and IL-12) on human NK cell cyt

37 wing stimulation with the combination of two monokines, IL-15 plus IL-12.

38 These monokines in turn favor expansion of Tc1 CD8+ T cells.

39 rgdorferi antigens modulated lymphokines and monokines in vitro.

40 mice produced more IFN-gamma in response to monokines in vivo than did NK cells from wild-type mice.

41 fer cells in association with the release of monokines including TNF, which causes activation of circ

42 Although monokines increased NK cell expression of the activating

43 r, IL-10, which is inhibitory for most other monokines, increased levels of IL-15 mRNA found after st

44 kin-12 (IL-12), since neutralization of this monokine increases susceptibility to infection.

45 Monocyte cytokines (ie, monokines) induce natural killer (NK) cells to produce i

46 on-inducible protein 10 [IP-10 (CXCL10)] and monokine induced by gamma interferon (IFN-gamma) [MIG (C

47 presented here demonstrate the expression of monokine induced by gamma interferon (IFN-gamma; Mig/CXC

48 oduction of interferon gamma (IFN-gamma) and monokine induced by gamma interferon (MIG) (CXCL9) in re

49 ly member 14 (TNFSF14, also known as LIGHT), monokine induced by gamma interferon (MIG), and granzyme

50 RANTES and eotaxin, and of the CXCR3 ligand monokine induced by gamma interferon (MIG).

51 phage inflammatory protein (MIP)-3alpha, and monokine induced by gamma interferon (MIG).

52 lated oncogene alpha [GRO-alpha], IP-10, and monokine induced by gamma interferon [MIG]), were upregu

53 in 3beta and proinflammatory chemokine CXCL9/monokine induced by gamma interferon in secondary lympho

54 vels of the Th1-associated chemokines CXCL9 (monokine induced by gamma interferon), CXCL10 (interfero

55 These studies revealed that Mig (monokine induced by gamma interferon), cytokine-responsi

56 chemokines interferon-inducible protein 10, monokine induced by gamma interferon, and platelet facto

57 , including interferon-inducible protein 10, monokine induced by gamma interferon, macrophage-induced

58 ificantly higher levels of chemokines KC and monokine induced by gamma interferon.

59 ], soluble tumor necrosis factor receptor-1, monokine induced by gamma interferon/chemokine [C-X-C mo

60 ines monocyte chemotactic protein-1/CCL2 and monokine induced by gamma interferon/CXCL9 in the hypote

61 ro-alpha, IFN-inducible protein-10, and mig (monokine induced by gamma-IFN), and of the adhesion mole

62 ed the expression and function of CXC (human monokine induced by gamma-interferon [HuMig], interleuki

63 -1), intercellular adhesion molecule-1, Mig (monokine induced by gamma-interferon), and RANTES (regul

64 IL-7, IL-8, IL-10, MCP-1, MCP-2, MCP-3, and monokine induced by gamma-interferon.

65 Monokine induced by gamma/chemokine (C-X-C motif) ligand

66 (10-kDa interferon-inducible protein), MIG (monokine induced by human interferon-gamma), and I-TAC (

67 ucible T cell alpha chemoattractant (I-TAC), monokine induced by IFN (Mig), and their receptor CXCR3

68 CXCL9 (monokine induced by IFN gamma [Mig]) and CXCL10 (interfe

69 ing mAbs to IFN-induced protein-10 (CXCL10), monokine induced by IFN-gamma (CXCL9), and IFN-inducible

70 IFN-gamma-inducible protein-10 (CXCL10), and monokine induced by IFN-gamma (CXCL9).

71 ial hemopoietic suppressive effects of human monokine induced by IFN-gamma (HuMig), a CXC chemokine t

72 In contrast, monokine induced by IFN-gamma (HuMig), which like HuIP-1

73 IP10 (OR 4.62, 95% CI 1.69-12.65, P = .003), monokine induced by IFN-gamma (MIG) (OR 3.11, 95% CI 1.1

74 The IFN-gamma-inducible proteins monokine induced by IFN-gamma (Mig) and chemokine respon

75 ed tumor cell clones that produce both CXCL9/monokine induced by IFN-gamma (Mig) and CXCL10/IFN-gamma

76 to mouse chromosome 5 close to the genes for monokine induced by IFN-gamma (MIG) and IP10.

77 This effect was associated with decreased monokine induced by IFN-gamma (Mig) and secondary lympho

78 hemokines IFN-gamma-inducible protein-10 and monokine induced by IFN-gamma (Mig) are expressed in all

79 n (IFN)-gamma-induced protein 10 (IP-10) and monokine induced by IFN-gamma (Mig) in a pool of human a

80 s IFN-gamma inducible protein 10 (IP-10) and monokine induced by IFN-gamma (Mig) in acute rejection o

81 n; peak levels of soluble TNF receptor 2 and monokine induced by IFN-gamma (MIG) on days 10-11 after

82 low or undetectable levels; and 2) IP-10 and monokine induced by IFN-gamma (Mig) were expressed in th

83 ets and the expression of its ligands CXCL9 (monokine induced by IFN-gamma (Mig)) and CXCL10 (IFN-gam

84 sion of T helper 1-associated CXCR3 ligands, monokine induced by IFN-gamma (Mig), and IFN-gamma-induc

85 nes IFN-inducible protein of 10 kDa (IP-10), monokine induced by IFN-gamma (Mig), and IFN-inducible T

86 N)-gamma-inducible protein of 10 kD (IP-10), monokine induced by IFN-gamma (Mig), and IFN-inducible T

87 hemokines--IFN-inducible protein 10 (IP-10), monokine induced by IFN-gamma (Mig), and IFN-inducible T

88 kines IFN-induced protein of 10 kDa (IP-10), monokine induced by IFN-gamma (Mig), and IFN-inducible T

89 k liver expression of another chemokine, the monokine induced by IFN-gamma (Mig), depended upon prese

90 1, interferon gamma-induced protein (IP)-10, monokine induced by IFN-gamma (MIG), epidermal growth fa

91 Expression of inducible protein (IP)-10, monokine induced by IFN-gamma (Mig), interferon inducibl

92 feron (IFN)-gamma inducible protein (IP)-10, monokine induced by IFN-gamma (Mig), interferon-inducibl

93 GF), IFN-gamma-inducible protein 10 (IP-10), monokine induced by IFN-gamma (MIG), monocyte chemotacti

94 the current study was to test the ability of monokine induced by IFN-gamma (Mig)-specific antibodies

95 emokines IFN-gamma inducible protein 10, and monokine induced by IFN-gamma (MIG).

96 IFN-gamma inducible protein-10 (IP-10) or to monokine induced by IFN-gamma (MIG).

97 The CXC chemokines (monokine induced by IFN-gamma (MIG)/CXC chemokine ligand

98 mmatory protein-10/CXC ligand (CXCL) 10, and monokine induced by IFN-gamma (MIG)/CXCL9 were significa

99 N-gamma and the IFN-gamma-induced chemokines monokine induced by IFN-gamma (Mig, CXCL9) and IFN-induc

100 ha-chemoattractant (I-TAC; CXCL11), and then monokine induced by IFN-gamma (Mig, CXCL9).

101 -gamma)-inducible protein 10 (IP-10/CXCL10), monokine induced by IFN-gamma (Mig/CXCL9), and interfero

102 n a radial diffusion assay, only recombinant monokine induced by IFN-gamma (MIG/CXCL9), IFN-gamma-ind

103 Monokine induced by IFN-gamma (Mig; CXC chemokine ligand

104 Monokine induced by IFN-gamma (MIG; CXC chemokine ligand

105 s of gamma interferon (IFN-gamma) and CXCL9 (monokine induced by IFN-gamma [MIG]) were found to be si

106 e expression of IFN-inducible protein 10 and monokine induced by IFN-gamma and cellular infiltration

107 elaboration of Th1 cytokines and chemokines monokine induced by IFN-gamma and IFN-gamma-inducible pr

108 protein of 10 kDa (IP-10), in contrast with monokine induced by IFN-gamma and IFN-inducible T cell-a

109 lity; (b) other ELR-negative CXC chemokines, monokine induced by IFN-gamma and platelet factor 4 that

110 rked induction of mRNAs for STAT1, IL-8, and monokine induced by IFN-gamma during the first day of tr

111 vation of IFN-gamma-inducible protein-10 and monokine induced by IFN-gamma expression in IFN-alpha-pr

112 hemokines IFN-gamma-inducible protein-10 and monokine induced by IFN-gamma in response to Klebsiella

113 tic increase in IFN-inducible protein 10 and monokine induced by IFN-gamma production.

114 inflammatory markers D-dimer, IFN-gamma, and monokine induced by IFN-gamma than i.v. challenged contr

115 The plasma levels of IL-17A, MCP-1, and monokine induced by IFN-gamma were increased in infants

116 Induced protein of 10 kDa and monokine induced by IFN-gamma were significantly elevate

117 ll alpha chemoattractant) (CXCL11), and Mig (monokine induced by IFN-gamma) (CXCL9), T-lymphocyte che

118 Conversely, the Th1-type chemokines, CXCL9 (monokine induced by IFN-gamma) and CXCL10 (IFN-gamma-ind

119 The CXCR3 ligands, CXCL9 (monokine induced by IFN-gamma) and CXCL10 (IFN-inducible

120 ounts of the IFN-inducible chemokines CXCL9 (monokine induced by IFN-gamma) and CXCL11 (IFN-gamma-ind

121 ; IP-10 (interferon-inducible protein); Mig (monokine induced by IFN-gamma) and decreased neutrophil

122 y that expression of the CXC chemokines Mig (monokine induced by IFN-gamma) and IP-10 (inducible prot

123 (IFN-gamma-inducible protein-10), and CXCL9 (monokine induced by IFN-gamma) and their corresponding c

124 or the T cell chemoattractant chemokine Mig (monokine induced by IFN-gamma) in contributing to a Th1

125 CL)10 (IFN inducible protein 10 kDa), CXCL9 (monokine induced by IFN-gamma), and CC chemokine ligand

126 Blocking of IP-10, but not monokine induced by IFN-gamma, aborts severity of Ag-spe

127 flagellin and IFN-inducible protein-10 kDa, monokine induced by IFN-gamma, and IFN-inducible T cell

128 L-8, RANTES, IFN-gamma inducible protein 10, monokine induced by IFN-gamma, and MIP-1alpha, specifica

129 h increased circulating levels of IFN-gamma, monokine induced by IFN-gamma, and RANTES.

130 matory cytokines IL-6, IL-12, CXCL10, MCP-1, monokine induced by IFN-gamma, and TNF-alpha in macropha

131 tractants IFN-gamma-inducible protein-10 and monokine induced by IFN-gamma, cellular infiltration int

132 (IFN-gamma)-inducible chemokine mRNAs (CXCL9/monokine induced by IFN-gamma, CXCL10/IFN-gamma-inducibl

133 CD4-depleted mice had lower levels of monokine induced by IFN-gamma, IFN protein-10 (IP-10), a

134 tokines and chemokines, including IFN-gamma, monokine induced by IFN-gamma, IFN-gamma-inducible prote

135 er levels than IFN-induced protein-10 or the monokine induced by IFN-gamma, it was the principal chem

136 Monokine induced by IFN-gamma, MCP-1, and IFN-gamma prod

137 hemokines IFN-gamma-inducible protein 10 and monokine induced by IFN-gamma, suggesting that macrophag

138 P-10, cutaneous T-cell-attracting chemokine, monokine induced by IFN-gamma, tumor necrosis factor-rel

139 enic chemokines IFN-inducible protein 10 and monokine induced by IFN-gamma.

140 interferon-inducible protein-10 (IP-10) and monokine induced by IFN-gamma.

141 vities of IFN-gamma inducible protein 10 and monokine induced by IFN-gamma.

142 hemokines IFN-gamma-inducible protein-10 and monokine induced by IFN-gamma.

143 the inflammatory chemokine receptors CXCR3 (monokine induced by IFN-gamma/CXC ligand (CXCL)9) and CX

144 CL11 mRNA in the CNS and decreased levels of monokine induced by IFN-gamma/CXCL9 mRNA in draining lym

145 y the other high affinity ligands for CXCR3, monokine induced by IFN-gamma/CXCL9, and I-TAC/CXCL11.

146 cells (IFN-inducible protein-10 kDa/CXCL10, monokine induced by IFN-gamma/CXCL9, IFN-inducible T cel

147 ssed IFNgamma-induced expression of the MIG (monokine induced by IFNgamma) gene, a C-X-C chemokine, i

148 (gamma-interferon-inducible protein (IP-10), monokine induced by INF-gamma (MIG), macrophage inflamma

149 tory protein 1alpha (MIP-1alpha), MIP-1beta, monokine induced by interferon (MIG)-gamma, and interfer

150 acrophage migration inhibitory factor (MIF), monokine induced by interferon gamma (MIG), and macropha

151 kines interferon gamma inducible protein 10, monokine induced by interferon gamma, and platelet facto

152 t concentrations of the CXCR3 ligands CXCL9 (monokine induced by interferon gamma, MIG) and CXCL10 (i

153 lasma cytokine production (interferon gamma, monokine induced by interferon gamma; P < 0.05) at day 1

154 , KC (mouse analog of interleukin-8 [IL-8]), monokine induced by interferon-gamma (CXCL9), and IL-1 r

155 colony-stimulating factor, stem cell factor, monokine induced by interferon-gamma (CXCL9), intercellu

156 )-inducible chemokine CXC chemokine ligand 9/monokine induced by interferon-gamma (CXCL9/Mig) was one

157 We combined IL-10 and monokine induced by interferon-gamma (derived from the 2

158 nflammatory protein-1Delta, osteoprotegerin, monokine induced by interferon-gamma (IFN), and IFN-gamm

159 , particularly the T-cell recruiting factors monokine induced by interferon-gamma (Mig) and inducible

160 FN-gamma inducible protein ([Crg2]IP-10) and monokine induced by interferon-gamma (Mig) are rapidly a

161 n-gamma-inducible protein-10 (IP-10) and the monokine induced by interferon-gamma (Mig) caused tissue

162 on-gamma-inducible 10-kd protein (IP-10) and monokine induced by interferon-gamma (MIG) constituted 2

163 feron-gamma inducible protein-10 (IP-10) and monokine induced by interferon-gamma (Mig) were determin

164 acrophage migration inhibitory factor (MIF), monokine induced by interferon-gamma (MIG), and matrix m

165 n-gamma-inducible protein of 10 kDa (IP-10); monokine induced by interferon-gamma (Mig); and regulate

166 odies (mAbs) to neutralize the CXCR3 ligands monokine induced by interferon-gamma (MIG, CXCL9) and in

167 Chemokines, including monokine induced by interferon-gamma (Mig/CXCL9), are pr

168 We hypothesized that the chemokine, monokine induced by interferon-gamma (MIG/CXCL9), which

169 fically, monocyte chemoattractant protein-1, monokine induced by interferon-gamma, and interferon-gam

170 es (interferon-inducible protein 10 [IP-10], monokine induced by interferon-gamma, and interferon-ind

171 nterferon-gamma-inducible protein-10 (IP10), monokine induced by interferon-gamma, and monocyte chemo

172 Mig, the monokine induced by interferon-gamma, is a CXC chemokine

173 kine (interferon-gamma-inducible protein-10, monokine induced by interferon-gamma, macrophage-inflamm

174 Of these transcripts, only four (human monokine induced by interferon-gamma, T-cell receptor ac

175 , macrophage inflammatory protein-1beta, and monokine induced by interferon-gamma.

176 as macrophage-colony-stimulating factor and monokine induced by interferon-gamma.

177 d by the CXC chemokine ligand 9 (CXCL9, Mig [monokine induced by interferon-gamma]) that impressively

178 ligands interferon-inducible protein 10 and monokine-induced by gamma interferon were detected on si

179 ding gamma-IFN-inducible protein (IP-10) and monokine-induced by gamma-IFN (MIG), as well as down-reg

180 d expression of IFN-inducible protein-10 and monokine-induced by IFN-gamma and thereby promote the co

181 cells secreted IFN-inducible protein-10 and monokine-induced by IFN-gamma in response to stimulation

182 e CXCR3 ligands IFN-inducible protein-10 and monokine-induced by IFN-gamma were selectively up-regula

183 feron-gamma inducible protein 10 (IP-10) and monokine-induced by IFN-gamma, (Mig), in allogeneic hear

184 ymphocytes correlated with both Th2 and Th1 (monokine-induced by IFN-gamma, IFN-gamma-inducible prote

185 CD94(high)CD56(dim) NK cells produce less monokine-induced IFN-gamma than CD56(bright) NK cells bu

186 emokine (MCP-1, macrophage-derived cytokine, monokine-induced IFN-gamma, keratinocyte-derived chemoki

187 ature effector cells, but also via bystander monokine-induced maturation of immature T cells.

188 demonstrate that SHIP1 negatively regulates monokine-induced NK cell IFN-gamma production in vitro a

189 NK cells temporally controls and limits the monokine-induced production of IFN-gamma, in part throug

190 coding IFN-gamma inducible protein of 10 kD, monokine inducible by gamma and RANTES.

191 n soluble tachyzoite antigen responsible for monokine induction are heat stable at 100 degree C but d

192 Together, these data argue that monokine induction by T. gondii is mediated by glycoprot

193 A further dichotomy in monokine induction signals was inferred from experiments

194 used to enumerate cytokine-producing cells (monokines: interleukin [IL]-1alpha, IL-1beta, IL-6, and

195 ne production may be governed in part by the monokine milieu induced during the early proinflammatory

196 t tumor necrosis factor-alpha (TNF-alpha), a monokine overexpressed in inflammatory myopathies, led t

197 es are shown to be dependent on the specific monokines present.

198 olerance, a state characterized by decreased monokine production and enhanced protection against endo

199 Notably, in the absence of significant monokine production by DenV-infected DC, it was the comb

200 Similarly, monokine production in vitro was reduced, whereas serum

201 ts of SLPI did not involve the modulation of monokine production since TNF-alpha and IL-10 were unaff

202 cytokines, regulated in part by differential monokine production.

203 itutively express monocyte-derived cytokine (monokine) receptors and secrete cytokines and chemokines

204 fector IFN-gamma(+) cells following a linear monokine-regulated pathway identical with that previousl

205 ction, whereas activation pathways for other monokine responses remain relatively intact.

206 an monocytes and suggest that stimulation of monokine secretion by bryo-1 may represent at least one

207 se to infection, monocyte-derived cytokines (monokines), stimulate natural killer (NK) cells to produ

208 ransduction 4 (STAT4), and STAT5 activity in monokine-stimulated NK cells, potentially contributing t

209 cantly enhanced IFN-gamma gene expression in monokine-stimulated NK cells.

210 SET was up-regulated upon monokine stimulation of primary human NK cells.

211 tor, IL-10, and IL-13 protein in response to monokine stimulation than do CD56(dim) NK cells, which p

212 d secrete cytokines and chemokines following monokine stimulation, and are therefore a critical compo

213 and may be predominantly an antiinflammatory monokine stimulus.

214 monocytes produce proinflammatory cytokines (monokines) such as interleukin (IL)-12, IL-15, and IL-18

215 Enhanced monokine synthesis requires engagement of P-selectin gly

216 ducible NO synthase, and multiple neutrophil/monokine-targeted chemokine programs.

217 ls produce far more IFN-gamma in response to monokines than do CD56dim NK cells.

218 nd monocytes and required both IL-17 and the monokines TNF-alpha and IL-1beta.

219 Conversely, CD14(+) monocytes synergize with monokines to promote IFN-gamma production by these NK ce

220 ependent IFN-gamma production in response to monokine treatment.

221 rs responsible for the induction of all four monokines were found to be sensitive to periodate oxidat