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1                                              VLA-1 expression, by immunohistochemistry, was increased
2 e alpha1beta1 integrin, very late antigen-1 (VLA-1), is a collagen receptor expressed in many CD4+ T
3                   Importantly, the activated VLA-1+ and VLA-1- cells can be isolated and maintained i
4                             The alpha1beta1 (VLA-1) integrin is a cell-surface receptor for collagen
5        Importantly, the activated VLA-1+ and VLA-1- cells can be isolated and maintained in culture a
6 ve intraperitoneal injections of VEGFR-3 and VLA-1-neutralizing antibodies or their controls twice a
7 ar endothelial growth factor receptor-3) and VLA-1 (very late antigen-1) promotes high-risk transplan
8 act as rapid effectors upon reinfection, and VLA-1 expression is integral to their accumulation in th
9 red to controls whereas alpha(v) subunit and VLA-1 were increased.
10                                 Alpha(v) and VLA-1 on intercellular junctions may participate in re-e
11 ent to and on luminal surfaces; alpha(v) and VLA-1 were on intercellular junctions.
12 nificantly less at day 32 in rats given anti-VLA-1 (P = 0.002).
13 educed in glomeruli and interstitium in anti-VLA-1-treated animals (P = 0.0006).
14                                      In anti-VLA-1-treated rats, serum creatinine was significantly l
15              Anti-VLA-5 (CD49e) but not anti-VLA-1 through VLA-4 and VLA-6, blocked the effect of Fn
16 a receptors, whereas anti-VLA-6 but not anti-VLA-1 through VLA-5 blocked the effect of Ln on IL-1 bet
17 d in the glomeruli of rats treated with anti-VLA-1.
18 6 and alpha(v) were the same as controls but VLA-1 remained increased.
19  alpha(1)beta(1) and alpha(2)beta(1) (CD49a, VLA-1 and CD49b, VLA-2, respectively), on CD4 and CD8 T
20 aques persistently elevated endothelial cell VLA-1 correlates with long-standing endothelial cell and
21 etimes expressing CD69 but not CD25, HLA-DR, VLA-1, or effector cytokines.
22 proximately 1-4% of the CD4+ T cells express VLA-1, and following T cell receptor activation ex vivo,
23 n-specific respiratory CD8 T cells expressed VLA-1, a marker that is associated with heterologous inf
24 th a recall antigen, are highly enriched for VLA-1+ cells.
25 he collagen-binding alpha(1)beta(1) integrin VLA-1 is essential for the development of memory CD8(+)
26                 The alpha 1 beta 1 integrin (VLA-1) is a major collagen/laminin receptor that regulat
27 t the collagen binding alpha1beta1 integrin, VLA-1, is expressed by the majority of influenza-specifi
28                 By immunoelectron microscopy VLA-1, VLA-6, beta1, and laminin were distributed throug
29                                    Moreover, VLA-1 gene depletion led to a marked inhibition of lymph
30 est the effect of systemic administration of VLA-1-neutralizing antibody on lymphatic formation and m
31  Antibody treatment or genetic deficiency of VLA-1 decreased virus-specific CTL in the lung and other
32 ure system was used to examine the effect of VLA-1 gene depletion on lymphatic endothelial cell funct
33 ing T cell activation favor the emergence of VLA-1+ cells.
34          Here we show that the expression of VLA-1 is a stable marker of a distinct subset of CD4+ me
35 Moreover, depletion of the small fraction of VLA-1+ cells present in CD4+ PBLs prior to stimulation s
36 lomerulonephritis and that neutralization of VLA-1, which enhanced expression of matrix metalloprotei
37 ceptor activation ex vivo, the percentage of VLA-1+ cells increases within the CD45RO+ population.
38                  We investigated the role of VLA-1 on virus-specific CD4(+) T cells during and after
39 alpha-chain of the type IV collagen receptor VLA-1, and these cells were highly activated, producing
40                           These data suggest VLA-1 expression defines a population of tissue memory C
41                             We conclude that VLA-1 mediates both glomerular and interstitial fibrosis
42  These novel findings together indicate that VLA-1 is critically involved in the processes of lymphan
43                           This suggests that VLA-1 is responsible for retaining protective memory CD8
44  data demonstrated, for the first time, that VLA-1 blockade significantly suppressed corneal lymphang
45              We propose that TNFR-II and the VLA-1 synergize to protect effector CD8 T cells in the i
46                                 Notably, the VLA-1+ cells in fresh CD4+ PBLs are composed of resting
47                          Interestingly, this VLA-1+ subset is enriched for Th1-type cells, and Th1-po
48                                        Thus, VLA-1 expression is a stable marker of a unique subset o
49 s and rats were given monoclonal antibody to VLA-1 (Ha31/8), 2.5 mg/kg, on alternate days.
50 e have examined the effect of an antibody to VLA-1 in crescentic glomerulonephritis.

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