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1 Genes encoding chemokines, including IL-8; macrophage inflammatory proteins 1, 3, and 4; and monocy
2 rmal T-cell expressed and Secreted (RANTES), macrophage inflammatory protein 1 alpha (MIP-1 alpha) an
3 e- and time-dependent manner, was strong for macrophage inflammatory protein 1 alpha (MIP-1 alpha) an
4 No significant changes in hepatic levels of macrophage inflammatory protein 1 alpha (MIP-1 alpha) or
5 arly disease stage was an increased level of macrophage inflammatory protein 1 alpha (MIP-1 alpha), a
7 a and was a weak inducer of IL-1 beta, IL-6, macrophage inflammatory protein 1 alpha (MIP-1 alpha), a
8 enic mice deficient in interleukin-6 (IL-6), macrophage inflammatory protein 1 alpha (MIP-1alpha), IL
9 eceptor alpha (IL-2Ralpha; CD25), CD40L, and macrophage inflammatory protein 1 alpha (MIP-1alpha).
10 monocyte chemotactic protein 1 [MCP-1], and macrophage inflammatory protein 1 alpha [MIP-1 alpha]) o
11 CC chemokines (CC chemokine ligand 3 [CCL3]/macrophage inflammatory protein 1 alpha [MIP-1 alpha], C
12 mokines (monocyte chemoattractant protein 1, macrophage inflammatory protein 1 alpha [MIP-1alpha], MI
13 ed and secreted), MIP-1alpha, and MIP-1beta (macrophage inflammatory protein 1 alpha and beta) could
14 released 36% less nitric oxide and 82% less macrophage inflammatory protein 1 alpha and expressed 63
15 ated genes in B cells were the CC chemokines macrophage inflammatory protein 1 alpha and macrophage i
16 he lower GT after infection, while the CCL3 (macrophage inflammatory protein 1 alpha) level was not i
17 locyte macrophage colony-stimulating factor, macrophage inflammatory protein 1 alpha, and tumor necro
18 pha and the mononuclear cell C-C chemokines: macrophage inflammatory protein 1 alpha, macrophage chem
19 the cytokines stromal cell-derived factor 1, macrophage inflammatory protein 1 alpha, or IL-1 beta.
20 chemoattractant protein 1, or MCP-1), CCL3 (macrophage inflammatory protein 1 alpha, or MIP-1 alpha)
21 lecules such as tumor necrosis factor alpha, macrophage inflammatory protein 1 alpha, transforming gr
22 inhibitory factor) and chemokines (eotaxin, macrophage inflammatory protein 1 alpha/beta, gamma inte
24 nd 22, CCL22), and anti-CCR5 factors include macrophage inflammatory protein-1 alpha (CCL3), macropha
25 ith other human CC chemokines, such as human macrophage inflammatory protein-1 alpha (hMIP-1 alpha) a
26 2-like receptors induces increased levels of macrophage inflammatory protein-1 alpha (MIP-1 alpha) an
27 athyroid hormone-related protein (PTHrP) and macrophage inflammatory protein-1 alpha (MIP-1 alpha) ar
28 ine at 10(-10)-10(-8) M and to the chemokine macrophage inflammatory protein-1 alpha (MIP-1 alpha) at
30 roduction of the T cell-attracting chemokine macrophage inflammatory protein-1 alpha (MIP-1 alpha) in
34 une responses in mice lacking CCR2, CCR5, or macrophage inflammatory protein-1 alpha (MIP-1 alpha), a
35 beta, and interleukin-1 alpha and chemokines macrophage inflammatory protein-1 alpha (MIP-1 alpha), M
36 other monocyte/macrophage-activating factor, macrophage inflammatory protein-1 alpha (MIP-1 alpha).
37 1ra), macrophage-derived chemokine (MDC) and macrophage inflammatory protein-1 alpha (MIP-1a) concent
38 ase-1 (TIMP-1) (p = 0.02) and an increase in macrophage inflammatory protein-1 alpha (MIP-1alpha) (p
39 okine induced by interferon gamma (MIG), and macrophage inflammatory protein-1 alpha (MIP-1alpha) wer
40 the role of proteoglycans in the function of Macrophage Inflammatory Protein-1 alpha (MIP-1alpha), a
41 es from 73 HIV-infected men were assayed for macrophage inflammatory protein-1 alpha (MIP-1alpha), MI
42 e growth inhibitory effects of the chemokine macrophage inflammatory protein-1 alpha (MIP-1alpha).
43 age chemotactic peptide-1, recombinant human macrophage inflammatory protein-1 alpha (rhMIP-1 alpha)
44 that the beta chemokines, recombinant human macrophage inflammatory protein-1 alpha and -1 beta, RAN
45 tochemical expression of the C-C chemokines, macrophage inflammatory protein-1 alpha and -beta, RANTE
46 ractant protein (gene product JE; MCP-1/JE), macrophage inflammatory protein-1 alpha and beta (MIP-1a
47 nificant elevation in interleukin-6, whereas macrophage inflammatory protein-1 alpha and monocyte che
48 VIP, IL-2, and IL-4, but only after 24 h for macrophage inflammatory protein-1 alpha and RANTES, as q
50 ere synthesized by astrocytic cells, whereas macrophage inflammatory protein-1 alpha and regulated on
51 CCL2/monocyte chemotactic protein 1 and CCL3/macrophage inflammatory protein-1 alpha) were also prese
52 covery that the beta-chemokines MIP-1 alpha (macrophage inflammatory protein-1 alpha), MIP-1 beta (ma
53 eratinocyte-derived chemokine); MIP-1 alpha (macrophage inflammatory protein-1 alpha); MCP-1 (monocyt
54 KC (an IL-8 homologue), MIG (CXCL9), RANTES, macrophage inflammatory protein-1 alpha, and eotaxin wer
55 n, normal T cell expressed and secreted) and macrophage inflammatory protein-1 alpha, beta-chemokines
56 mokines (monocyte chemoattractant protein-1, macrophage inflammatory protein-1 alpha, interferon-gamm
58 ation normal T cell expressed and secreted), macrophage inflammatory protein-1 alpha, macrophage infl
59 ls of the chemotactic factors interleukin-5, macrophage inflammatory protein-1 alpha, monocyte chemoa
62 study demonstrates that the beta-chemokines macrophage inflammatory proteins 1 alpha and 1 beta (MIP
63 e (chemoattractant cytokines) beta peptides, macrophage inflammatory proteins 1 alpha and 1 beta (MIP
64 okines similar to the cell lines, as well as macrophage inflammatory proteins 1 alpha and 1 beta.
65 beta, macrophage-inflammatory protein 2, and macrophage-inflammatory protein 1 alpha, all regulators
68 inophilia accompanied by local production of macrophage-inflammatory protein-1 alpha (MIP-1 alpha).
69 rophage-inflammatory protein-1 beta (but not macrophage-inflammatory protein-1 alpha), monocyte-chemo
70 in-10, monokine induced by interferon-gamma, macrophage-inflammatory protein-1 alpha, and regulated o
71 hage CSF, basic fibroblast growth factor, or macrophage-inflammatory protein-1 alpha, and was associa
72 chemokine ligand (CCL)2), and immature DCs (macrophage-inflammatory protein-1 alpha/CCL3, macrophage
74 ch as stromal-cell-derived factor 1 (SDF-1), macrophage inflammatory protein 1-alpha (MIP-1alpha), an
75 ed expression of T-cell-attracting chemokine macrophage inflammatory protein 1-alpha (MIP-1alpha/CCL3
76 -gamma induced protein 10 (IP-10; p = 0.02), macrophage inflammatory protein 1-alpha (MIP-1alpha; p =
77 o) mice have increased circulating levels of macrophage inflammatory protein 1-alpha and interleukin-
78 on against chemotactic gradient generated by macrophage inflammatory protein 1-alpha or monocyte chem
79 te macrophage colony-stimulating factor, and macrophage inflammatory protein 1-alpha were lower 14 da
80 roinflammatory cytokines interleukin-1alpha, macrophage inflammatory protein 1-alpha, and interleukin
81 ytic polypeptide 3 G/F/H) and CC chemokines (macrophage inflammatory protein 1-alpha, macrophage infl
84 thyroid hormone-related protein (PTHrP), and macrophage inflammatory protein-1-alpha (MIP-1alpha), ha
85 f inflammation as measured by interleukin 6, macrophage inflammatory protein 1 and 2 expression, pres
86 levels of proinflammatory markers, including macrophage inflammatory proteins 1 and 2 and interleukin
88 was partially competed by the beta-chemokine macrophage inflammatory protein 1 beta (MIP-1 beta) and
89 icantly reduced the binding and signaling of macrophage inflammatory protein 1 beta (MIP-1 beta) usin
90 ral consequences of N-terminal truncation in macrophage inflammatory protein 1 beta (MIP-1 beta), a C
91 C3; and an increase in the levels of CD107a, macrophage inflammatory protein 1 beta (MIP-1beta), and
92 monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 1 beta (MIP-1beta), and
93 vated endothelium by its capacity to trigger macrophage inflammatory protein 1 beta from primary mono
94 rferon (IFN)-gamma-inducible protein 10, and macrophage inflammatory protein 1 beta levels were diffe
95 of PD-1 expression were required to inhibit macrophage inflammatory protein 1 beta production, lower
96 Interleukin 8 (IL-8), K60 (a CXC chemokine), macrophage inflammatory protein 1 beta, and IL-1 beta le
97 on of mRNAs for tumor necrosis factor alpha, macrophage inflammatory protein 1 beta, interleukin 6, a
98 ls IRF-5 stimulates transcription of RANTES, macrophage inflammatory protein 1 beta, monocyte chemota
99 ressed), monocyte chemoattractant protein 1, macrophage inflammatory protein 1 beta, secondary lympho
102 rophage inflammatory protein-1 alpha (CCL3), macrophage inflammatory protein-1 beta (CCL4), and RANTE
103 chemoattractant protein-1 (MCP-1), IL-8, and macrophage inflammatory protein-1 beta (MIP-1 beta)).
104 -1 receptor antagonist [IL-1Ra], IL-6, IL-8, macrophage inflammatory protein-1 beta [MIP-1beta]/C-C m
105 yte-macrophage colony-stimulating factor and macrophage inflammatory protein-1 beta levels in cocultu
106 whereas the levels of IL-6, IL-8, IL-10, and macrophage inflammatory protein-1 beta were higher in pa
107 e inflammatory protein-1 alpha), MIP-1 beta (macrophage inflammatory protein-1 beta) and RANTES (regu
109 interleukin-2, tumor necrosis factor-alpha, macrophage inflammatory protein-1 beta, and CD107a by CD
110 onse to HIV antigens, CD8 cell production of macrophage inflammatory protein-1 beta, or ELISPOT assay
111 es (macrophage inflammatory protein-1 alpha, macrophage inflammatory protein-1 beta, RANTES, and IFN-
112 , since 125I-labeled RANTES was displaced by macrophage-inflammatory protein-1 beta (but not macropha
113 genesis to identify amino acids of chemokine macrophage-inflammatory protein-1 beta (MIP-1 beta) that
114 acrophage-inflammatory protein-1 alpha/CCL3, macrophage-inflammatory protein-1 beta/CCL4), but not ch
115 es (macrophage inflammatory protein 1-alpha, macrophage inflammatory protein 1-beta, regulated on act
116 lysis, we found expression of the chemokine, macrophage inflammatory protein-1 delta (MIP-1 delta), t
118 mic proinflammatory chemokine levels such as macrophage inflammatory protein-1-gamma, B-lymphocyte ch
119 r functions; cardiac inflammation (increased macrophage inflammatory protein 1, interleukin-1, P-sele
120 o 3-fold greater amounts of IL-18, TNFalpha, macrophage inflammatory protein 1, macrophage inflammato
121 HMG-CoA synthase), aldehyde dehydrogenase 2, macrophage inflammatory protein 1 (MIP-1) and neurotensi
122 tors monocyte chemotactic protein-1 (MCP-1), macrophage inflammatory protein 1 (MIP-1), and macrophag
123 flammatory cytokines such as interleukin-15, macrophage inflammatory protein 1 (MIP-1), and RANTES (r
124 ral latent ORF73, immunomodulatory K5, viral macrophage inflammatory protein 1 (MIP-1), and viral MIP
125 L-1beta, interferon-gamma inducible protein, macrophage inflammatory protein-1 (MIP-1) alpha, and MIP
126 matopoiesis, including interleukin-3 (IL-3), macrophage inflammatory protein-1 (MIP-1), and thrombosp
128 similarly to LTB(4), C5a, and the chemokines macrophage inflammatory protein-1 (MIP-1)alpha or MIP-2,
129 IL-6, as well as the migration-related genes macrophage inflammatory protein-1 (MIP-1alpha), MIP-2 an
130 TES, monocyte chemotactic protein-1 (MCP-1), macrophage inflammatory protein-1 (MIP-1beta), and MCP-3
131 in mRNA expression of three beta chemokines, macrophage-inflammatory protein 1 (MIP-1) alpha (CCL3),
132 related oncogene alpha (GROalpha), GROgamma, macrophage inflammatory protein 1, monocyte chemoattract
133 ulmonary and activation-regulated chemokine; macrophage inflammatory protein-1, regulated upon activa