ライフサイエンスコーパス: MIP-1beta

1 MIP-1beta expression in beta-cells was verified by doubl

2 MIP-1beta levels remain elevated in GT2/3 patients who a

3 MIP-1beta, a member of the chemokine family of proteins,

4 MIP-1beta, granulocyte colony-stimulating factor (G-CSF)

5 MIP-1beta-induced G-protein activation was further incre

6 mmatory protein (MIP)-1alpha/CCL3 (P<0.001), MIP-1beta/CCL4, and vascular endothelial growth factor (

7 01), MDC (P < .001), MIP-1alpha, (P < .001), MIP-1beta (P = .005), MCP-1 (P = .03), and TNF-alpha (P

8 , 7.1] vs 32.6 pg/ml [7.1, 88.0]; p = .001), MIP-1beta (30.7 pg/ml [30.7, 30.7] vs 243.3 pg/ml [30.7,

9 MCP-1 (monocyte chemoattractant protein-1), MIP-1beta, and RANTES (regulated on activation normal T

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

11 cible protein-10, and also shows that MCP-1, MIP-1beta, and IL-1beta can potentially distinguish path

12 ignificantly higher concentrations of MCP-1, MIP-1beta, and IL-1beta in patients compared with EC, wh

13 d with controls, mean serum levels of MCP-1, MIP-1beta, and IL-8 were all much higher in patients wit

14 n 2 (MIP-2), monocyte chemotactic protein 1, MIP-1beta, inducible protein 10, and T-cell activation g

15 proinflammatory molecules including VCAM-1, MIP-1beta, and MIP-2 in response to LTbetaR ligation.

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

17 okine genes, such as those encoding CXCL-13, MIP-1beta, RANTES, and IL-8.

18 crophage inflammatory protein (MIP)-1alpha , MIP-1beta , monocyte chemotactic protein 1, thymus-and-a

19 ge inflammatory protein-1alpha (MIP-1alpha), MIP-1beta, and growth-related oncogene beta (GRO-beta).

20 ge inflammatory protein-1alpha (MIP-1alpha), MIP-1beta, and IL-9, as well as IL-10, more commonly con

21 ge inflammatory protein 1alpha (MIP-1alpha), MIP-1beta, and RANTES by primary human microglia after e

22 ge inflammatory protein 1alpha (MIP-1alpha), MIP-1beta, and RANTES, interfere with HIV-1 binding to C

23 ge inflammatory protein-1alpha (MIP-1alpha), MIP-1beta, and the murine homolog of Gro(alpha), i.e. KC

24 ge inflammatory protein 1alpha (MIP-1alpha), MIP-1beta, hepatocyte growth factor (HGF), IFN-gamma-ind

25 ge inflammatory protein-1alpha (MIP-1alpha), MIP-1beta, MIP-2, and monocyte chemoattractant protein-1

26 ge inflammatory protein 1alpha (MIP-1alpha), MIP-1beta, MIP-2, interferon gamma-inducible protein, mo

27 ge inflammatory protein 1alpha (MIP-1alpha), MIP-1beta, monokine induced by interferon (MIG)-gamma, a

28 ge inflammatory protein 1alpha (MIP-1alpha), MIP-1beta, RANTES, and members of the monocyte chemotact

29 acrophage inflammatory protein (MIP) 1alpha, MIP-1beta, and VEGF, and found that the pattern and leve

30 acrophage inflammatory protein (MIP)-1alpha, MIP-1beta, and IFN-gamma inducible protein-10 than did c

31 acrophage inflammatory protein (MIP)-1alpha, MIP-1beta, and IL-8.

32 acrophage-inflammatory protein (MIP)-1alpha, MIP-1beta, and MIP-2 were increased, whereas regulated o

33 acrophage inflammatory protein (MIP)-1alpha, MIP-1beta, and RANTES (regulated on activation, normally

34 acrophage inflammatory protein (MIP)-1alpha, MIP-1beta, interleukin (IL)-8, and interferon-gamma-indu

35 acrophage inflammatory protein (MIP)-1alpha, MIP-1beta, IP-10, and interleukin-6.

36 acrophage-inflammatory protein (MIP)-1alpha, MIP-1beta, MIP-2, MIP-3alpha, thymus- and activation-reg

37 acrophage inflammatory protein (MIP)-1alpha, MIP-1beta, monocyte chemoattractant protein (MCP)-1, int

38 macrophage inhibitory protein (MIP)-1alpha, MIP-1beta, monocyte chemotactic protein 1, and RANTES (r

39 thermore, it increased levels of MIP-1alpha, MIP-1beta, and CCR5 transcripts in the cornea and conjun

40 ost chemokines, including MIP-2, MIP-1alpha, MIP-1beta, and eotaxin, tended to decline with age.

41 a poor correlation between IL-8, MIP-1alpha, MIP-1beta, and GRO-beta mRNA levels and protein producti

42 interleukin-8 (IL-8), Exodus II, MIP-1alpha, MIP-1beta, and IL-1alpha and preferentially expressed ge

43 cytokines (including chemokines MIP-1alpha, MIP-1beta, and IP-10).

44 hase (Nos2), lipocalin-2 (Lcn2), MIP-1alpha, MIP-1beta, and keratinocyte-derived cytokine (KC), were

45 ein-coupled receptor for RANTES, MIP-1alpha, MIP-1beta, and MCP-2 that functions as the front line co

46 IL-10, IL-6, MIP-1alpha, MIP-1beta, and MCP-2 were associated with increased odds

47 The CC chemokines MIP-1alpha, MIP-1beta, and RANTES and their receptors CCR1 and CCR5

48 The MIP-1alpha, MIP-1beta, and RANTES chemokines are natural ligands of

49 ymphocyte chemokines IP-10, MIG, MIP-1alpha, MIP-1beta, and RANTES were decreased in the lungs of inf

50 ating levels of beta-chemokines (MIP-1alpha, MIP-1beta, and RANTES) and their respective transcriptio

51 etion of chemokines (MDC, I-309, MIP-1alpha, MIP-1beta, and RANTES), cytokines (gamma interferon, tum

52 IFN-gamma and TNF-alpha but not MIP-1alpha, MIP-1beta, and RANTES.

53 ed IL-4, IL-5, IL-13, TNF-alpha, MIP-1alpha, MIP-1beta, and RANTES.

54 suppressed the levels of MIP-2, MIP-1alpha, MIP-1beta, and RANTES.

55 l to generate IFN-gamma, GM-CSF, MIP-1alpha, MIP-1beta, and RANTES.

56 Expression of mRNA for RANTES, MIP-1alpha, MIP-1beta, and SDF-1 and secretion of the chemokines int

57 ion of IFN-gamma, GM-CSF, IL-13, MIP-1alpha, MIP-1beta, CCL5, and TNF-alpha, and massive release of c

58 in pulmonary neutrophilia, IL-6, MIP-1alpha, MIP-1beta, CXCL1, and CXCL5 in AlloTbet mice.

59 (TGF-beta1), TGF-beta2, RANTES, MIP-1alpha, MIP-1beta, IL-8, and PF-4 were identified in media condi

60 ntly increased concentrations of MIP-1alpha, MIP-1beta, IP-10, and MIG proteins in the corneal epithe

61 de IL-1beta, IL-6, IL-10, MCP-1, MIP-1alpha, MIP-1beta, MMP-2, and TNF-alpha.

62 -17, Eotaxin, IP-10, MIG, MCP-1, MIP-1alpha, MIP-1beta, RANTES, tumor necrosis factor (TNF)-alpha, in

63 RNA and protein for MIP-2, CINC, MIP-1alpha, MIP-1beta, TNF-alpha, and IL-1beta.

64 acrophage inflammatory protein [MIP]-1alpha, MIP-1beta), hematopoietic IL-7, and granulocyte macropha

65 acrophage inflammatory protein [MIP]-1alpha, MIP-1beta, all p < or = 0.001, but no change in growth-r

66 acrophage inflammatory protein [MIP]-1alpha, MIP-1beta, and RANTES [regulated on activation, normally

67 Expression of MIP-1alpha; MIP-1beta; regulated on activation, normal T-cell expres

68 e inflammatory protein 1 alpha [MIP-1alpha], MIP-1beta) were significantly diminished or even nonexis

69 ge inflammatory protein 1alpha [MIP-1alpha], MIP-1beta, RANTES) and CXC families (growth-related onco

70 tory protein-1alpha (MIP-1alpha) and -1beta (MIP-1beta), lymphotactin), b) type-2-dominant (eotaxin,

71 okine macrophage inflammatory protein 1beta (MIP-1beta) and inducible nitric oxide synthase 2.

72 ibits macrophage inflammatory protein 1beta (MIP-1beta) binding properties that are distinct from CCR

73 7a or macrophage inflammatory protein 1beta (MIP-1beta) expression from HIV-1-specific T cells.

74 P-1), macrophage inflammatory protein 1beta (MIP-1beta), and serum amyloid A protein (SAA) during acu

75 -10), macrophage inflammatory protein 1beta (MIP-1beta), and soluble interleukin 2Ralpha (sIL-2Ralpha

76 CL20, macrophage inflammatory protein 1beta (MIP-1beta), CXCL-13, and RANTES.

77 nd 6, macrophage inflammatory protein 1beta (MIP-1beta), interleukin 8 (IL-8), monocyte chemotactic p

78 , and macrophage inflammatory protein 1beta (MIP-1beta).

79 , and macrophage inflammatory protein 1beta (MIP-1beta).

80 , and macrophage inflammatory protein 1beta (MIP-1beta).

81 se in macrophage inflammatory protein 1beta (MIP-1beta; CCL4) and monocyte chemoattractant protein 2

82 okine macrophage inflammatory protein 1beta (MIP-1beta; CCL4) did not cause chemotaxis, but CCL4 was

83 okine macrophage inflammatory protein-1beta (MIP-1beta) by placing a disulfide bond at the center of

84 kine, macrophage inflammatory protein-1beta (MIP-1beta) production.

85 MDC), macrophage inflammatory protein-1beta (MIP-1beta), and C10 from eosinophils.

86 pha), macrophage inflammatory protein-1beta (MIP-1beta), and CD107 in addition to interferon-gamma (I

87 in 1, macrophage inflammatory protein 1beta [MIP-1beta], and MIP-3alpha) as early as 1 h after exposu

88 , and macrophage inflammatory protein-1beta [MIP-1beta]) in both normal monocytes and in the THP-1 mo

89 y mediators (interleukin-6 [IL-6], IL-1beta, MIP-1beta, tumor necrosis factor alpha [TNF-alpha], and

90 ha, macrophage-inflammatory protein (MIP)-2 (MIP-1beta), and IL-8 by LPS-stimulated neutrophils was a

91 acterized effector markers (IFN-gamma, IL-2, MIP-1beta, TNF, CD107a, and perforin) were identified by

92 ory protein-1alpha/CCL-3 (MIP-1alpha/CCL-3), MIP-1beta/CCL-4, and RANTES/CCL-5, among others.

93 IL-13-induced chemokines (MIP-1alpha/CCL-3, MIP-1beta/CCL-4, MIP-2/CXCL-1, RANTES/CCL-5), MMP-2, -9,

94 ect CC and CXC chemokines (MIP-1alpha/CCL-3, MIP-1beta/CCL-4, MIP-2/CXCL2/3, MCP-1/CCL-2, MCP-2/CCL-8

95 lpha)/CCL3 [chemokine (C-C motif) ligand 3], MIP-1beta/CCL4, RANTES (regulated on activation, normal

96 Asbestos also caused increases in IL-4, MIP-1beta, and MCP-1 in BALF that were more elevated (p

97 increased percentage of NK cells producing a MIP-1beta response to pH1N1 virus compared with nonpregn

98 Mutations in this domain abrogated MIP-1beta induction but did not affect other Nef-ascribe

99 ignature (PS; IL-2(+)IFN-gamma(+)TNF-alpha(+)MIP-1beta(+)) found at low levels among NC.

100 gnature (NPS; IL-2(-)IFN-gamma(+)TNF-alpha(-)MIP-1beta(+)), found at increased levels among NC; and (

101 f cells that expressed IFN-gamma, TNF-alpha, MIP-1beta, and combinations of these cytokines.

102 levels of IL-2, IL-6, IFN-gamma, TNF-alpha, MIP-1beta, IL-1, IL-12, IL-13, and IL-10 were measured i

103 IL-6, TNF-alpha, MIP-1beta, MCP-1, iNOS/NOS2, CD11b, CD68, CD4 and CD8 mR

104 /- 35 pg/mL vs 41 +/- 9 pg/mL; P < 0.01) and MIP-1beta (950 +/- 418 pg/mL vs 125 +/- 32 pg/mL; P < 0.

105 hemokines monocyte chemotactic protein-1 and MIP-1beta in a manner that was dependent on MAPK activat

106 levels of monocyte chemotactic protein-1 and MIP-1beta.

107 , IL-13, IFNgamma, G-CSF, GM-CSF, MCP-1, and MIP-1beta compared with controls.

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

109 ing cytokine secretion, especially IL-10 and MIP-1beta.

110 factor (TNF)-alpha, IL-1ra, IL-2, IL-13, and MIP-1beta (macrophage inflammatory protein-1beta) respon

111 NF-alpha, IL-1beta, and IL-6, MIP-1alpha and MIP-1beta also were significantly higher in cells treate

112 creased circulating levels of MIP-1alpha and MIP-1beta and decreased RANTES.

113 resistant EC cells contained MIP-1alpha and MIP-1beta and was sufficient to confer R5-tropic resista

114 ted that Met-RANTES inhibited MIP-1alpha and MIP-1beta at 50% inhibition concentrations of 5 nM and 2

115 ophage inflammatory protein (MIP)-1alpha and MIP-1beta at week 8.

116 Baseline MIP-1alpha and MIP-1beta did not significantly differ between children

117 Both MIP-1alpha and MIP-1beta form high-molecular-weight aggregates.

118 ymerization process and human MIP-1alpha and MIP-1beta form rod-shaped, double-helical polymers.

119 ed that heterodimerization of MIP-1alpha and MIP-1beta is specific and that it occurs at physiologica

120 Peripheral blood MIP-1alpha and MIP-1beta levels were significantly elevated in mild and

121 MIP-1alpha and MIP-1beta mRNAs were also upregulated in F43-inoculated

122 characterized the affects of MIP-1alpha and MIP-1beta on cellular and humoral immune responses.

123 -Ba stimulated high levels of MIP-1alpha and MIP-1beta production in elutriated monocytes and even hi

124 otein complex containing both MIP-1alpha and MIP-1beta under normal conditions from culture supernata

125 ophage inflammatory protein (MIP)-1alpha and MIP-1beta were critical for their homing.

126 ophage inflammatory protein (MIP)-1alpha and MIP-1beta were markedly induced in the infarcted mouse m

127 CCL3 and CCL4 (also known as MIP-1alpha and MIP-1beta) are produced.

128 ory protein 1alpha and 1beta (MIP-1alpha and MIP-1beta) now have been shown to be secreted from activ

129 ime points, the expression of MIP-1alpha and MIP-1beta, but not of Ltn, was restored despite the inhi

130 ory protein 1alpha and 1beta (MIP-1alpha and MIP-1beta, respectively) secretion was observed primaril

131 ophage inflammatory protein (MIP)-1alpha and MIP-1beta.

132 and triggering the release of MIP-1alpha and MIP-1beta.

133 inflammatory protein-1alpha (MIP-1alpha) and MIP-1beta are distinct but highly homologous CC chemokin

134 inflammatory protein-1alpha (MIP-1alpha) and MIP-1beta.

135 nflammatory protein-1alpha (MIP-1alpha), and MIP-1beta are the natural ligands of the HIV-1 corecepto

136 nflammatory protein-1alpha (MIP-1alpha), and MIP-1beta, the pattern of which varied by stimulant.

137 flammatory protein 1-alpha (MIP-1alpha), and MIP-1beta, which chemoattract genetically modified BMCs

138 nflammatory protein-1alpha (MIP-1alpha), and MIP-1beta.

139 s of beta-chemokines RANTES, MIP-1alpha, and MIP-1beta because (i) supernatants greatly inhibited the

140 LPS-induced IL-6, TNF-alpha, MIP-1alpha, and MIP-1beta expression in human primary monocytes.

141 lpha interferon (IFN-alpha), MIP-1alpha, and MIP-1beta in plasmacytoid DCs (pDCs) exposed to RSV afte

142 induced expression of MCP-1, MIP-1alpha, and MIP-1beta mRNA in the retinal vessels 3 hours after repe

143 -gamma-inducible protein-10, MIP-1alpha, and MIP-1beta mRNA transcripts, had greater numbers of CD11b

144 Expression of KC, MIP-1alpha, and MIP-1beta mRNA was equivalent in C57BL/6 allogeneic skin

145 ated increased levels of KC, MIP-1alpha, and MIP-1beta protein at day 4 posttransplant that were decr

146 phage inflammatory protein (MIP)-1alpha, and MIP-1beta than the control cells.

147 phage inflammatory protein (MIP)-1alpha, and MIP-1beta were all rapidly induced and sensitive to cycl

148 phage-inflammatory protein (MIP)-1alpha, and MIP-1beta with donor-dependent changes in monocyte chemo

149 ), chemokines (IL-8, RANTES, MIP-1alpha, and MIP-1beta) and transcription factors (early growth respo

150 L-1beta], IL-6, IL-8, MCP-1, MIP-1alpha, and MIP-1beta) was detected at either the protein or message

151 phage inflammatory protein (MIP)-1alpha, and MIP-1beta, account for the suppression of R5 HIV by bloc

152 nterleukin-8 (IL-8), RANTES, MIP-1alpha, and MIP-1beta, whereas only IL-8 and RANTES were induced fol

153 phage inflammatory protein (MIP)-1alpha, and MIP-1beta.

154 pression of IL-1beta, MIP-2, MIP-1alpha, and MIP-1beta.

155 phage inflammatory protein (MIP)-1alpha, and MIP-1beta], and complement component C5a in bronchoalveo

156 production of IFN-gamma, TNF-alpha, IL-2 and MIP-1beta were significantly increased in LMNCs, in cont

157 he cytokines IFN-gamma, TNF-alpha, IL-2, and MIP-1beta.

158 he chemokines IP-10, MCP-1, MCP-3, MCP-5 and MIP-1beta, which in turn augmented offspring postnatal h

159 oduction of IFN-gamma, TNF-alpha, CCL-5, and MIP-1beta.

160 Induction of IL-8 and MIP-1beta was confirmed at the transcriptional level by

161 ocked the production of TNF-alpha, IL-8, and MIP-1beta in response to leukotriene D(4).

162 f proinflammatory cytokines (IL-6, IL-8, and MIP-1beta) by monocytes and DCs (IC50 < 1 muM) and preve

163 mg/kg), transient increases in TNF-alpha and MIP-1beta serum concentrations and NK cell CD69 expressi

164 roduction of IL-2, IFN-gamma, TNF-alpha, and MIP-1beta alone or in combination, following activation

165 cell expression of IL-1beta, TNF-alpha, and MIP-1beta, respectively (P < 0.01 [2019 versus B29]).

166 roduction of IFN-gamma, IL-2, TNF-alpha, and MIP-1beta.

167 receptor and its ligands MIP-1alpha/CCL3 and MIP-1beta/CCL4.

168 ory protein-1 (MIP-1), MIP-1alpha (CCL3) and MIP-1beta (CCL4) are chemokines crucial for immune respo

169 oteins MIP-1alpha, MIP-1alphaP (CCL3L1), and MIP-1beta; granulocyte-macrophage colony-stimulating fac

170 the chemokines MCP-1/CCL2, RANTES/CCL5, and MIP-1beta/CCL4 (1).

171 tion exceeded that in the mono-cultures, and MIP-1beta declined significantly compared with MPhi cult

172 ally restricted to vascular endothelium, and MIP-1beta+ macrophages were found throughout the section

173 , and significant induction of IFN-gamma and MIP-1beta, all indicative of an effective, albeit insuff

174 mmatory mediators IL-6, IL-8, IFN-gamma, and MIP-1beta, as well as of the regulatory cytokine IL-10,

175 rituximab, rituximab-F(ab')2, or medium and MIP-1beta, IL-10, interferon-gamma, and tumor necrosis f

176 ed NFAT activation, ERK phosphorylation, and MIP-1beta production.

177 in CCR5(-/-) mice and blockade of RANTES and MIP-1beta, but not in CCR1(-/-), CCR2(-/-)/MIP-1alpha(-/

178 secretion of IL-8, IL-6, MCP-1, RANTES, and MIP-1beta, but not TNF-alpha, whereas AMs secreted TNF-a

179 Addition of human anti-MIP-1beta neutralizing antibody or a specific inhibitor

180 Treatment of anti-MIP-1beta and anti-MCP-1 significantly delayed the onset

181 enic mediators, including chemokines such as MIP-1beta (CCL-4), lymphotactin (XCL-1), IFN-gamma-induc

182 tors, lactacystin and epoxomicin, attenuated MIP-1beta induced CCR5 down-modulation as detected by fl

183 ificant associations between higher baseline MIP-1beta levels and smaller decreases in MIP-1beta earl

184 -1), macrophage inflammatory protein 1 beta (MIP-1beta), and interleukin-18 (IL-18) in 131 patients w

185 07a, macrophage inflammatory protein 1 beta (MIP-1beta), and TNF-alpha from NK cells.

186 L-8, macrophage inflammatory protein-1 beta [MIP-1beta]/C-C motif chemokine ligand 4 [CCL4], interfer

187 In studies of glycosaminoglycan binding, MIP-1beta-A10C binds to a heparin-Sepharose column as ti

188 ation of select chemokines (MIP-1alpha/CCL3, MIP-1beta/CCL4, MCP-1/CCL-2), matrix metalloproteinase-9

189 ammatory protein-1alpha (MIP-1alpha)), CCL4 (MIP-1beta), CCL5 (RANTES), CXCL2 (MIP-2), and CXCL10 (in

190 kines CCL2 (MCP-1), CCL3 (MIP-1alpha), CCL4 (MIP-1beta), CCL5 (RANTES), and CXCL10 (IP-10), and promo

191 lpha that was induced by IL-15; and 4) CCL4 (MIP-1beta), also induced by IL-15, had a significant inh

192 oters, the human CCL3 (MIP-1alpha) and CCL4 (MIP-1beta), were transfected into human chondrocytes wit

193 d TNF, and chemokines CCL2 (MCP-1) and CCL4 (MIP-1beta).

194 Cxcl2 (MIP-2), Ccl3 (MIP-1alpha), and Ccl4 (MIP-1beta).

195 ion of high levels of CCL3/MIP-1alpha, CCL4/ MIP-1beta, and CCL5/RANTES but not of CXCL12/SDF-1.

196 L5/RANTES, CCL11/eotaxin-1, CCL2/MCP-1, CCL4/MIP-1beta, CCL7/MCP-3, and CCL20/MIP3alpha protein level

197 , IL-1beta, TNF-alpha, CCL3/MIP-1alpha, CCL4/MIP-1beta, and CXCL1/KC production, which resulted in in

198 0.02 muM HagB-induced CCL3/MIP-1alpha, CCL4/MIP-1beta, and TNFalpha responses.

199 alpha (TNF-alpha), CCL3/MIP-1alpha, and CCL4/MIP-1beta production and lower neutrophil recruitment, y

200 ibitory chemokines, CCL3/MIP-1alpha and CCL4/MIP-1beta, were induced in human primary monocytes when

201 chemokines CXCL8/IL-8, CCL2/MCP-1, and CCL4/MIP-1beta.

202 d at onset of clinical uveitis, whereas CCL4/MIP-1beta was elevated at the peak of AU.

203 -regulation of MIP-1alpha/CCL3, RANTES/CCL5, MIP-1beta/CCL4, and MCP-1/CCL2 chemokines.

204 , we found a significant reduction in CD107a/MIP-1beta expression in HIV-1-specific CD8(+) T cells.

205 ed expression of neutrophil chemoattractants MIP-1beta and keratinocyte chemoattractant and the neutr

206 st definitive evidence that the CC chemokine MIP-1beta dimer is not able to bind or activate its rece

207 idated the GAG binding site of the chemokine MIP-1beta and implicated the involvement of the chemokin

208 s vCCI in complex with a human CC chemokine, MIP-1beta (macrophage inflammatory protein 1beta).

209 lammatory protein (MIP)-2, the CC chemokines MIP-1beta and MIP-1alpha, and the cytokines TNF-alpha an

210 1 increased the expression of the chemokines MIP-1beta or CCL4.

211 N-gamma, TNF-alpha and IL-6) and chemokines (MIP-1beta) in decidual and placental cells.

212 produced abundant amounts of CC chemokines (MIP-1beta, MIP-1alpha, and RANTES) but not IL-2.

213 he generation of proinflammatory chemokines (MIP-1beta, IL-8, and MCP-1) by hMCs by a mechanism that

214 In contrast, MIP-1beta, whose receptor is CCR5, did not induce signif

215 Correspondingly, MIP-1beta produced higher titers of Ag-specific mucosal

216 (K(92)EK) that is required for Nef-dependent MIP-1beta production by infected macrophages.

217 Higher early MIP-1beta levels were also significantly associated with

218 Plasma IL-2, eotaxin, MIP-1beta, and IL-15 and semen eotaxin and granulocyte c

219 For MIP-1beta F13Y, the presence of the disaccharide increas

220 The affinity of the CD4-CCR5 complex for MIP-1beta was 3.5-fold lower than for CCR5, but the inte

221 ned a total of 940 structural restraints for MIP-1beta F13A, and have calculated a family of structur

222 nterestingly, mucosally derived T cells from MIP-1beta-treated mice displayed higher levels of IL-4 a

223 Furthermore, MIP-1beta- and MCP-2-producing cells and CD4+ T cells we

224 olyfunctional response pattern of IFN-gamma, MIP-1beta and TNF-alpha.

225 T-cell functions (degranulation, IFN-gamma, MIP-1beta, TNF-alpha, and IL-2) simultaneously in chroni

226 HGF, GRO, MIP-1beta, IL-1alpha, TGF-beta1, and TGF-beta2 may play

227 However, MIP-1beta-A10C neither binds nor activates the MIP-1beta

228 Evaluation of analogues in the (125)I-[MIP-1beta] binding and Ba-L-HOS antiviral assays resulte

229 cell subset that synthesizes MIP-1beta; (ii) MIP-1beta and IFN-gamma are synthesized congruently in m

230 IL-2-producing cells, and least abundant in MIP-1beta-producing MTB-specific CD4 T cells from HIV-in

231 ne MIP-1beta levels and smaller decreases in MIP-1beta early in treatment and SVR.

232 infected cells gave significant increases in MIP-1beta, IL-28A, MCP-2, and IFN-alpha as compared with

233 e dramatic effect of the absence of Phe13 in MIP-1beta, we used multidimensional heteronuclear NMR to

234 BMCs to HRV 16-infected cells did not induce MIP-1beta, IL-28A and IFN-alpha efficiently nor did it d

235 ET-1-induced MIP-1beta expression involved hypoxia-inducible factor-1

236 cleotide augmented several-fold ET-1-induced MIP-1beta expression.

237 Moreover, ET-1-induced MIP-1beta mRNA expression in either THP-1 cells or perip

238 ET-1-induced MIP-1beta mRNA expression in THP-1 cells and human perip

239 ET-1-induced MIP-1beta promoter luciferase activity was attenuated wh

240 e inhibitory effect of PGE(2) on LPS-induced MIP-1beta production.

241 caused substantial inhibition of NGF-induced MIP-1beta production both in the absence and presence of

242 approximately 30% inhibition of NGF-induced MIP-1beta production but had no effect on priming by C3a

243 Rituximab-induced MIP-1beta secretion depends on the combined presence of

244 hat synthesize MIP-1beta lack perforin; (iv) MIP-1beta is synthesized with approximately equal freque

245 ater amounts of interleukin-13 but much less MIP-1beta and interleukin-6 than bone marrow-derived cul

246 CXCR4 ligand SDF-1alpha and the CCR5 ligand MIP-1beta.

247 d transfection with one of the CCR5 ligands, MIP-1beta (CCL4), increased their resistance against HIV

248 down-modulated by their respective ligands, MIP-1beta/SDF-1alpha or by the HIV envelope protein, gp1

249 her, these studies showed that ET-1-mediated MIP-1beta gene expression is regulated via hypoxia-respo

250 less mature, and most produced IL-2 but not MIP-1beta.

251 ot appear to be necessary for the ability of MIP-1beta to function on its receptor CCR5, as enzymatic

252 ted ADCC and antibody-mediated activation of MIP-1beta in NK cells as the four immunological paramete

253 e dramatically, the dimerization affinity of MIP-1beta L34W also increases upon addition of disacchar

254 duced very little IL-2, but large amounts of MIP-1beta.

255 d LAD2 cells, LTD4 induced the generation of MIP-1beta, a response blocked by short hairpin RNA-media

256 onstrate substantial subset heterogeneity of MIP-1beta synthesis among CD8(+) T cells and suggest tha

257 nly led to significantly increased levels of MIP-1beta in co-cultures of B and NK cells.

258 Levels of MIP-1beta were higher in patients with a high affinity F

259 After this effect for the mutants of MIP-1beta was shown, similar experiments were conducted

260 significantly increased T-cell production of MIP-1beta and polyfunctionality in NK and T cells to pH1

261 ile were: (a) the simultaneous production of MIP-1beta, TNF-alpha, and IFN-gamma in the absence of IL

262 inding site in the 3' untranslated region of MIP-1beta mRNA.

263 which targets the 3' untranslated region of MIP-1beta RNA.

264 regions being similar, the up-regulation of MIP-1beta, TNF-alpha, IFN-gamma, and ICAM-1 and the loss

265 beta-sheet II to interact with a surface of MIP-1beta that includes residues adjacent to its N termi

266 ng several dimerization-impaired variants of MIP-1beta (F13Y, F13L, L34W, and L34K), these studies in

267 to investigate the effect of GAG binding on MIP-1beta dimerization.

268 GAGs from cells results in little effect on MIP-1beta activity.

269 aled that antibodies to either MIP-1alpha or MIP-1beta precipitated a protein complex containing both

270 ophages toward MCP-1, RANTES, MIP-1alpha, or MIP-1beta, as well as cell adhesion to ICAM-1 or fibrone

271 Splenic T cells from MIP-1alpha- or MIP-1beta-treated mice displayed higher Ag-specific Th1

272 te TrkA phosphorylation, NFAT activation, or MIP-1beta production.

273 ed increased production of MIP-1alpha and/or MIP-1beta at the protein level.

274 rived macrophages with either HIV-1 gp120 or MIP-1beta results in the CCR5-mediated activation of Lyn

275 t on SDF-1alpha-induced p44/42 MAP kinase or MIP-1beta-induced p38 kinase activities, thus indicating

276 or NF-kappaB binding motifs in the proximal MIP-1beta promoter (-1053/+43 bp) were mutated.

277 es (IL-1beta, IL-5, IL-6, TNF-alpha, RANTES, MIP-1beta, MCP-1, KC and IL-10).

278 nt number of CD8(+) T cells contained stored MIP-1beta that was released after HBa stimulation.

279 ce through a single amino acid substitution (MIP-1beta-A10C).

280 ly 60% of the CD8(+) T cells that synthesize MIP-1beta lack perforin; (iv) MIP-1beta is synthesized w

281 e predominant T cell subset that synthesizes MIP-1beta; (ii) MIP-1beta and IFN-gamma are synthesized

282 e susceptible to HIV infection in vitro than MIP-1beta-producing cells.

283 P-1beta-A10C neither binds nor activates the MIP-1beta receptor CCR5.

284 accumulation of CD4+ Th cells expressing the MIP-1beta/MCP-2 receptor, CCR5, in the lungs of mice.

285 ract with positively charged residues in the MIP-1beta N terminus, 20s region and 40s loop.

286 rmine the three-dimensional structure of the MIP-1beta F13A variant.

287 the role of GAGs in the manipulation of the MIP-1beta quaternary structure.

288 ining the same mutation, suggesting that the MIP-1beta dimer participates in heparin binding.

289 TNF, MIP-1beta, and MIP-1alpha were produced predominantly by

290 ith enhanced in vitro chemotaxis response to MIP-1beta (CCL4).

291 olecules in the asymmetric unit comprise two MIP-1beta-like dimers.

292 D28(-) subpopulations of CD8(+) T cells; (v) MIP-1beta is synthesized by three distinct CD8(+) T cell

293 Previously, our structure of the vCCI.MIP-1beta (macrophage inflammatory protein-1beta) comple

294 binding pattern is very similar to the vCCI.MIP-1beta complex and suggest that electrostatic interac

295 -alpha, IL-6, IL-12p70, IL-10, GM-CSF, VEGF, MIP-1beta, TNF-beta, IFN-alpha2 and IL-7 in response to

296 the expression of CD45R0 and CD62L; and (vi) MIP-1beta is not synthesized in short-term cultures of n

297 e that DCP induced mycobacterial killing via MIP-1beta- and nitric oxide-dependent effects.

298 by IgG2a and IgG3 subclass responses, while MIP-1beta only stimulated IgG1 and IgG2b subclasses.

299 unoglobulin G (IgG) and IgM responses, while MIP-1beta promoted lower IgG and IgM but higher serum Ig

300 led that this association was increased with MIP-1beta stimulation.