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1 tor, and chemokines mediating neutrophil and monocyte infiltration.
2 e to both resident macrophage activation and monocyte infiltration.
3 (BBB), and are cleared without neutrophil or monocyte infiltration.
4 neurysm in ApoE(-/-) mice partly by reducing monocyte infiltration.
5 ctions in microglial activation and cerebral monocyte infiltration.
6 liver injury, steatosis, and proinflammatory monocyte infiltration.
7 d with a dramatic decrease in neutrophil and monocyte infiltration.
8 stic of HIV-1 that influences HAD, increased monocyte infiltration.
9 eactive responses of retinal glial cells and monocyte infiltration.
10 n between chemokine expression and placental monocyte infiltration.
11 l malaria and were associated with placental monocyte infiltration.
12 s (GA) characterized by recipient T cell and monocyte infiltration.
13 osis, are characterized by compartmentalized monocyte infiltration.
14  chemoattractants associated with glomerular monocyte infiltration.
15 vascular macrophages severely hampered Ly6C+ monocyte infiltration.
16 of resident macrophages or a result of blood monocyte infiltration.
17 n circulating monocytes, directly inhibiting monocyte infiltration.
18 sident macrophage homeostasis, and triggered monocyte infiltration.
19 icroglia activation and PR degeneration with monocyte infiltration.
20 ng neutrophils or by genetically suppressing monocyte infiltration.
21 modulating the complement cascade and muscle monocyte infiltration.
22               We previously showed that host monocyte infiltration and activation within the graft dr
23 l CCR2/CCR5 inhibitor, cenicriviroc) reduces monocyte infiltration and APAP-induced liver injury (AIL
24 ent focal ischemia, Cxcr4 deficiency reduces monocyte infiltration and blunts the expression of patte
25 icle mice had marked increases in macrophage/monocyte infiltration and fibrosis of the left ventricle
26 atic cancer, characterized by CD4 T cell and monocyte infiltration and high copy number variation bur
27  however, the spatiotemporal distribution of monocyte infiltration and its correlation to prognostic
28 DCs accumulated in the heart coincident with monocyte infiltration and loss of resident reparative em
29                                              Monocyte infiltration and macrophage formation are pivot
30 cardiomyocytes, thereby attenuating Ly6C(hi) monocyte infiltration and myocardial inflammation.
31 effects associated with reduced inflammatory monocyte infiltration and neutrophil activation in the l
32 ow that TLR5 agonist, flagellin, can promote monocyte infiltration and osteoclast maturation directly
33 on of 07/2a mAb with FUS-BBBD led to greater monocyte infiltration and recruitment to plaques in this
34 t microglia are key regulators of peripheral monocyte infiltration and retinal pigment epithelium mig
35   Intratumor enrichment of eATP promotes the monocyte infiltration and stimulates their production of
36                                              Monocyte infiltration and subsequent differentiation int
37  stroke, we find that Cxcr4 promotes initial monocyte infiltration and subsequent territorial restric
38 mune landscape characterised by inflammatory monocyte infiltration and the generation of 'mono-macs'.
39 utaneous collagen mRNA, which is preceded by monocyte infiltration and the up-regulation of cutaneous
40 proliferative glomerulonephritis with marked monocyte infiltration and, at times, intracapillary thro
41                                              Monocytes' infiltration and differentiation into monocyt
42 d less crescent formation, tubular dilation, monocyte infiltration, and interstitial renal fibrosis.
43  diminished macrophage activation, decreased monocyte infiltration, and reduced production of inflamm
44 d that VEGF regulates vascular permeability, monocyte infiltration, and scar-associated macrophages f
45 pment by decreasing steatosis, liver damage, monocyte infiltration, and the production of inflammator
46  by a loss of smooth muscle cells, increased monocyte infiltration, and the reprograming of myofibrob
47 ic lung T(RM)s to determine whether CCR2 and monocyte infiltration are essential for vaccine-induced
48 d.nNOS had a particularly striking impact on monocyte infiltration; as early as 24 hours after gene t
49                                Inhibition of monocyte infiltration at the induction phase of experime
50 inhibits translation and attenuates Ly6C(hi) monocyte infiltration by inhibiting a proinflammatory re
51 istration of GM-CSF exacerbated inflammatory monocyte infiltration by upregulating CCL2 expression, r
52  findings suggest that strategies that limit monocyte infiltration can potentiate vaccine-induced fro
53     Collectively our data suggest that early monocyte infiltration causes permanent changes to microg
54  macrophages has reinforced the concept that monocyte infiltration dictates macrophage buildup.
55 ding to endothelial cell (EC) activation and monocyte infiltration during antibody-mediated rejection
56                  To test the hypothesis that monocyte infiltration during atherogenesis is MCP-1 depe
57 76 (2007)] indicated a consistent pattern of monocyte infiltration during T. gondii infection to the
58          To elucidate the regulation of this monocyte infiltration, expression of monocyte chemoattra
59 to the RPE layer, followed by (2) subsequent monocyte infiltration from the retinal vasculature into
60                                At 3 sites of monocyte infiltration/giant cell formation (granulation
61    These findings suggest a crucial role for monocyte infiltration, giving rise to macrophages or oth
62 mice of both sexes, we found that preventing monocyte infiltration improves the neurogenic and prolif
63 ed significantly impaired CCL2 secretion and monocyte infiltration in an experimental model of perito
64    Using this strain, we effectively abolish monocyte infiltration in genetically engineered murine m
65                                 The impaired monocyte infiltration in MVO regions could be related to
66 ion of rPSGL-1-Ig abolished antibody-induced monocyte infiltration in the allograft, but had little e
67 n markedly increased neutrophil, T-cell, and monocyte infiltration in the diseased brain.
68 lly, skin expansion increases macrophage and monocyte infiltration in the skin while altering systemi
69 M activates complement cascade and increased monocyte infiltration in the soleus muscle, which was am
70  in CNS-infiltrating lymphocytes and reduced monocyte infiltration in the trigeminal afferent pathway
71 -1(-/-) mice exhibited significantly reduced monocyte infiltration in wire injury-induced neointima a
72 nhibited both resident ATM proliferation and monocyte infiltration into adipose tissue and decreased
73 ced activity of the NRF2 pathway and reduced monocyte infiltration into adipose tissue may underlie i
74 st the impact of PM(2.5) in eliciting direct monocyte infiltration into fat, we rendered FVBN mice ex
75 d less monocyte-derived cells, less Ly6c(hi) monocyte infiltration into lesions, and lower levels of
76 hemotactic protein-1 (MCP-1) is critical for monocyte infiltration into the arterial wall and neointi
77 inical and clinical results demonstrate that monocyte infiltration into the brain after myocardial in
78                                              Monocyte infiltration into the CNS is a hallmark of seve
79 ing SIV infection, which was associated with monocyte infiltration into the dorsal root ganglia (DRG)
80 G3 should have a greater capacity to trigger monocyte infiltration into the graft than IgG2 or IgG4 d
81    Interestingly, blockade of CCR2-dependent monocyte infiltration into the heart reduced soluble MER
82 mulate pathobiological processes involved in monocyte infiltration into the mesangium.
83                                    Recently, monocyte infiltration into the placental intervillous sp
84 ils and two stages of GR1+CD68+ inflammatory monocyte infiltration into the site of inoculation.
85  further increased the degree of circulating monocyte infiltration into the tissue matrix.
86                                              Monocyte infiltration into the vessel wall, a key initia
87                                              Monocyte infiltration into these areas appeared 24 h lat
88 ein-coupled chemokine receptors, it promotes monocyte infiltration into tissues in response to the ch
89                                              Monocyte infiltration is implicated in a variety of dise
90 nded on the level of chemokine secretion and monocyte infiltration; low-level MCP-1 secretion with mo
91 -inflammatory cytokine signaling, peripheral monocyte infiltration, microglial activation, and hypoth
92 e histologically analyzed for neutrophil and monocyte infiltration, neovascularization and epithelial
93 n of endothelial adhesion molecules limiting monocyte infiltration of the artery wall.
94  CFU of Brucella spp. display neutrophil and monocyte infiltration of the joint space and surrounding
95  Low density lipoprotein (LDL) oxidation and monocyte infiltration of the vessel wall underlie athero
96 cyte infiltration (CD43-positive cells), and monocyte infiltration (RAM-11-positive cells).
97 ation; low-level MCP-1 secretion with modest monocyte infiltration resulted in tumor formation, where
98 phase of NASH development by promoting blood monocyte infiltration through the production of IP-10 an
99  mRNA network that controls inflammation and monocyte infiltration to the myocardium.
100 lodronate treatment or inhibition of gastric monocyte infiltration using the Cx3cr1 knockout mouse mo
101                            Notably, limiting monocyte infiltration via genetic Ccl2 reduction prolong
102                       In the absence of MVO, monocyte infiltration was more intense in MI regions wit
103 ce imaging performed in series revealed that monocyte infiltration was spatially inhomogeneous in rep
104                 The distribution patterns of monocyte infiltration were correlated to the presence of
105 Atherosclerotic lesions are characterized by monocyte infiltration, which may be regulated by the che
106 terized histologically by tubular injury and monocyte infiltration, while the stable posttransplant s

 
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