ライフサイエンスコーパス: MCP-3

1 but enhanced levels of CC chemokines (MCP-1, MCP-3).

2 and MCP-1, respectively, but both shared by MCP-3.

3 with other C-C chemokines such as MCP-1 and MCP-3.

4 hage inflammatory protein-1 (MIP-1beta), and MCP-3.

5 these receptors, CCR2B, binds both MCP-l and MCP-3.

6 unique opportunity to evaluate the role for MCP-3.

7 production in response to MCP-1, MCP-2, and MCP-3.

8 ced a significantly lower level of MCP-1 and MCP-3.

9 JNK in FFA-induced upregulation of MCP-1 and MCP-3.

10 hemokine receptor that responds to MCP-1 and MCP-3.

11 al cells were an important in situ source of MCP-3.

12 hysiological agonists eotaxin-1, RANTES, and MCP-3.

13 lux in response to the chemokines RANTES and MCP-3.

14 th neutralizing antibodies demonstrated that MCP-3 abrogated eosinophil accumulation in type-2 lesion

15 re than 60% sequence homology with MCP-1 and MCP-3 and about 30% homology with macrophage inflammator

16 -3, MCP-5, or MCP-2 plus MCP-5 revealed that MCP-3 and MCP-1 are the CCR2 agonists most critical for

17 Our data demonstrate that MCP-3 and MCP-1 provide parallel contributions to CCR2-m

18 hat PAR-1 is important for the production of MCP-3 and MCP-5.

19 We identified three chemokines, MCP-1, MCP-3 and MRP-1, which are negatively regulated by BCL-6

20 so abolished the eosinophil Ca2+ response to MCP-3 and partially desensitized the response to macroph

21 ond class of lower affinity ligands includes MCP-3 and possibly two other viral chemokines.

22 expressed in AML14.3D10 cells bound eotaxin, MCP-3 and RANTES with Kds of 0.1, 2.7 and 3.1 nM, respec

23 chemoattractant protein-1 and -3 (MCP-1 and MCP-3) and mouse JE and FIC are potent activators of mon

24 , IL-13, monocyte chemoattractant protein-3 (MCP-3), and eotaxin expression.

25 (RANTES) and monocyte chemotactic protein 3 (MCP-3), and the anaphylatoxin C5a, induce activation, de

26 /eotaxin-1, CCL2/MCP-1, CCL4/MIP-1beta, CCL7/MCP-3, and CCL20/MIP3alpha protein levels increased duri

27 multaneously increasing expression of MCP-1, MCP-3, and cytolysin.

28 ell as local reductions of TNF-alpha, MCP-1, MCP-3, and eotaxin.

29 E cells resulted in the modulation of MCP-1, MCP-3, and IL-8.

30 se of eosinophils to eotaxin, RANTES, MCP-2, MCP-3, and MCP-4 was shown to be mediated through CCR3.

31 mokine gradients (mainly CCL11, CCL24, CCL5, MCP-3, and MCP-4), cell surface expression of adhesion m

32 ANTES, monocyte chemotactic protein (MCP)-2, MCP-3, and MCP-4.

33 The CCR2 ligands MCP-1, MCP-3, and MCP-5 are detected in bone marrow and in seru

34 Three ligands for CCR2 (MCP-1, MCP-3, and MCP-5) were upregulated during Fr98 infection

35 ands monocyte chemotactic protein 1 (MCP-1), MCP-3, and MCP-5, as well as RANTES and growth-related o

36 out increased mRNA for CCR2 agonists, MCP-1, MCP-3, and MCP-5, but reduced IL-4 and IFNgamma mRNA.

37 F4/80(+) cells as major producers of MCP-1, MCP-3, and MCP-5.

38 CCR2, which responds to murine MCP-1, MCP-2, MCP-3, and MCP-5.

39 IL-5, IL-6, IL-7, IL-8, IL-10, MCP-1, MCP-2, MCP-3, and monokine induced by gamma-interferon.

40 tro that was blocked by anti-RANTES and anti-MCP-3 antibodies.

41 id not compensate for the loss of MCP-1, and MCP-3 appears to be a less effective mediator of monocyt

42 monocyte chemotactic protein 1 (MCP-1), and MCP-3 but not IL-12.

43 MCP-2 binding was competed for by MCP-1 and MCP-3, but less well by MIP-1alpha or RANTES.

44 Eotaxin, RANTES, and to a lessor extent MCP-3, but not the other chemokines, activated CC CKR3 a

45 ll chemotaxis assays to eotaxin, RANTES, and MCP-3, but not to any other chemokines.

46 The enhanced expression of Fn14 and MCP-3 by 12% stretch and the enhanced expression of Col1

47 e mouse lungs had reduced expression of CCL7/MCP-3, CC11/eotaxin-1, and CCL24/eotaxin-2.

48 (CCL-5), and monocyte chemotactic protein-3 (MCP-3, CCL-7) and 4 (MCP-4, CCL-13) are potent eosinophi

49 -4, MIP-2/CXCL2/3, MCP-1/CCL-2, MCP-2/CCL-8, MCP-3/CCL-7, MCP-5/CCL-12, KC/CXCL-1, and Lix/CXCL-5), m

50 the CCR2 ligands MCP-1 (CCL2), MCP-2 (CCL8), MCP-3 (CCL7), MCP-4 (CCL13), and eotaxin (CCL11), as wel

51 tractant protein-1 (MCP-1/CCL2), but neither MCP-3/CCL7 nor MCP-5/CCL12, were significantly elevated

52 yte chemoattractant protein (MCP)-1/CCL2 and MCP-3/CCL7 on their ability to bind GAGs.

53 Monocyte chemotactic protein-3 (MCP-3/CCL7) has potent eosinophil chemoattractant proper

54 ensin 2, monocyte chemoattractant protein-3 (MCP-3/CCL7) or macrophage-derived chemokine (MDC/CCL22),

55 kine receptor, CCR2 (MCP-1/CCL2, MCP-2/CCL8, MCP-3/CCL7, MCP-4/CCL13, and Eotaxin/CCL11), and the CCR

56 e CC chemokines, MCP-1/CCL2, MCP-2/CCL8, and MCP-3/CCL7, with HS-derived oligosaccharides.

57 was correlated with the diminished MCP-1 and MCP-3 chemokine production and decreased blood and liver

58 lta) macrophages; however, the production of MCP-3, coded by the immediate downstream gene, was signi

59 Together, these results suggest that MCP-3 contributes to a significant component of eosinoph

60 The effects of MCP-3 could be diminished by a neutralizing antibody to

61 <0.01), IL-7 (P<0.05), IL-8/CXCL8 (P<0.001), MCP-3/CXCCL7 (P<0.05) and MIP-1alpha/CCL-3 (P<0.05) were

62 hibition of adenylate cyclase and MCP-1- and MCP-3-driven cytosolic calcium influx; the compounds are

63 Others (MCP-2, MCP-3, eotaxin, lymphotactin, LARC, TCA-3) displayed pea

64 In contrast, levels of MCP-3, eotaxin-1, and CCR3 transcripts increased in both

65 Monocyte chemotactic protein-3 (MCP-3)/fibroblast-induced cytokine (FIC), a CC chemokine

66 Pretreatment of mice with an anti-MCP-3/FIC Ab significantly inhibited the OVA-induced air

67 The expression of MCP-3/FIC and other CC chemokines (MCP-1, macrophage inf

68 We conclude that MCP-3/FIC plays a significant role in the allergen-induc

69 allergen challenge induced the expression of MCP-3/FIC predominantly in the airway epithelium.

70 Immunocytochemical staining for MCP-3/FIC showed that the allergen challenge induced the

71 -regulated the expression of mRNA for MCP-1, MCP-3/FIC, and macrophage inflammatory protein-1alpha at

72 of airway inflammation to study the role of MCP-3/FIC.

73 und that the monocyte chemotactic protein 3 (MCP-3) gene expression was significantly induced by infe

74 n of the monocyte chemoattractant protein 3 (MCP-3) gene, which promoted chemotaxis of preosteoclasts

75 , IL-6, and IL-12b), chemokines (MIP-1alpha; MCP-3; growth-related oncogenes 1 and 2; and inflammator

76 Several receptors for MCP-1 and MCP-3 have been cloned from human monocytic cell lines,

77 Surprisingly, eotaxin (IC(50) = 6.7 nM) and MCP-3 (IC(50) = 4.1 nM) bind with greater affinity than

78 in 8 (IL-8), monocyte chemotactic protein 3 (MCP-3), IL-2 receptor beta (IL-2Rbeta), IL-15 receptor a

79 trate, for the first time, overexpression of MCP-3 in early-stage SSc and in Tsk1 skin, and suggest a

80 calization confirmed increased expression of MCP-3 in the dermis of 4 of 5 Tsk1 skin samples and 14 o

81 t L. monocytogenes infection rapidly induces MCP-3 in tissue culture macrophages and in serum, spleen

82 r-reporter gene constructs were activated by MCP-3 in transgenic mice and by transient transfection a

83 chemoattractant protein (MCP)-1, MCP-2, and MCP-3, in hepatic fibrosis.

84 ds, and the extended structures of MCP-1 and MCP-3 increase in abundance upon activation.

85 ncludes increase of IL-5, IL-13, eotaxin and MCP-3; infiltration of eosinophils into the airway submu

86 MIP-1beta, MIP-1alpha, RANTES, eotaxin, and MCP-3 (ligands for CCR5 and/or CCR3) revealed the presen

87 nocyte chemotactic protein-2 (MCP-2) and -3 (MCP-3), liver and activation-regulated chemokine (LARC),

88 Immunohistochemical staining revealed that MCP-3 localized to vessels in or near granulomas suggest

89 motactic protein (MCP)-1 and RANTES (but not MCP-3), macrophage inflammatory protein (MIP)-1alpha, MI

90 moattractant protein-1 and protein-3 (MCP-1, MCP-3), macrophage-inflammatory protein-1beta (MIP-1beta

91 closely related monomeric chemokines (MCP-1, MCP-3, MCP-4, and eotaxin) and, subsequently, utilize th

92 ha), monocyte-chemotactic protein-1 (MCP-1), MCP-3, MCP-4, and eotaxin.

93 as observed for six other chemokines (MCP-1, MCP-3, MCP-4, RANTES (regulated on activation normal T c

94 milk levels of the chemokines IP-10, MCP-1, MCP-3, MCP-5 and MIP-1beta, which in turn augmented offs

95 Some of these chemokines as well as RANTES, MCP-3, MCP-5, and cytokine-response gene-2 (CRG-2)/IFN-i

96 monocyte chemoattractant protein-1 (MCP-1), MCP-3, MCP-5, or MCP-2 plus MCP-5 revealed that MCP-3 an

97 hese findings provide evidence that CCR2 and MCP-3/MCP-1 are critical for monocyte mobilization and s

98 ed [RANTES], monocyte chemotactic protein-3 [MCP-3], MCP-4, IL-8, interferon-inducible protein-10, ma

99 Hepatic CCR2, MCP-1, MCP-2, and MCP-3 messenger RNA expression was increased after bile

100 MCP-3(-/-) mice clear bacteria less effectively from the

101 MCP-3(-/-) mice have significantly fewer Ly6C(high) mono

102 MCP-3(-/-) mice, like MCP-1(-/-) mice, have fewer TNF- a

103 icited in mice immunized with DNA expressing MCP-3 or beta-defensin 2 fusion constructs.

104 ncreased but subsequently reduced by RANTES, MCP-3, or C5a.

105 e was no compensatory upregulation of MCP-2, MCP-3, or MCP-5 in MCP-1-null mice with EAE.

106 significant decrease in MCP-1 (P < 0.01) and MCP-3 (P < 0.05), but a significant increase in IL-8 (P

107 (vitronectin and fibronectin), inflammatory (MCP-3, PF-4, and MIP-1alpha) and immunomodulatory (gamma

108 Thus, up-regulated MCP-3 production did not compensate for the loss of MCP-

109 The up- and down-regulation of MCP-3 production in MCP-1(Delta/Delta) and MCP-1 KO mice

110 Despite the increased MCP-3 production in MCP-1(Delta/Delta) mice, thioglycola

111 e lung endothelial cells displayed augmented MCP-3 production in response to interleukin-4.

112 Decreased MCP-3 production was also detected in previously generat

113 Altered MCP-1 and/or MCP-3 production was also observed in vivo in each mouse

114 Expression of MCP-3 protein was assessed by Western blotting of fibrob

115 a, IFN response genes, and chemokines MCP-1, MCP-3, RANTES (regulated on activation, normally T cell-

116 ssenger ribonucleic acids (mRNAs) for MCP-1, MCP-3, RANTES, MIP-1alpha, and IL-8 were produced by BAL

117 e polymerase chain reaction (PCR) for MCP-1, MCP-3, RANTES, MIP-1alpha, IL-8, and beta-actin.

118 ologous chemoattractant, and only RANTES and MCP-3 showed mutual inhibition.

119 nly cytosol invasive L. monocytogenes induce MCP-3, suggesting that cytosolic innate immune detection

120 ression of IL-13 and some degree of IL-5 and MCP-3, suggesting that these cytokines could potentially

121 ng to CCR3 are mimicked on the eotaxin-1 and MCP-3 surface.

122 f vMIP-II to those of eotaxin-1, RANTES, and MCP-3, three CCR3 physiological agonists with known thre

123 ll recruiting (G-CSF, IL-1beta, IL-8, MCP-1, MCP-3, TNF-alpha), polarizing (CXCL13, IL-10, IL-13, IL-

124 Maximal MCP-3 transcript expression was abrogated by anti-interl

125 Both MCP-3 transcripts and protein levels were more strongly

126 Activation of collagen reporter genes by MCP-3 was explored in transgenic mouse fibroblasts and b

127 MCP-3 was highly overexpressed by neonatal Tsk1 fibrobla

128 tion of eosinophils to FMLP, C5a, RANTES, or MCP-3 was totally inhibited by the presence of the homol

129 age-inflammatory protein-1alpha, eotaxin, or MCP-3 were instilled into the airways of normal mice or

130 Immunoreactivity for eotaxin, RANTES, and MCP-3 were not detected.

131 s of MCP-1 and MCP-5, and moderate levels of MCP-3, when stimulated with recombinant IFN-alpha in cul

132 rked accumulation of mRNA for both MCP-1 and MCP-3, which are known to suppress IL-12 production in L

133 This receptor also bound RANTES and MCP-3 with high affinity, but not other CC or CXC chemok

134 RANTES, and monocyte chemotactic protein-3 (MCP-3) with high affinity (K(i) ranged from 1 nm to 5.5

135 netically stimulated migration to RANTES and MCP-3, without stimulating random migration.