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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
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
16 a receptors, whereas anti-VLA-6 but not anti-VLA-1 through VLA-5 blocked the effect of Ln on IL-1 bet
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
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
25 he collagen-binding alpha(1)beta(1) integrin VLA-1 is essential for the development of memory CD8(+)
27 t the collagen binding alpha1beta1 integrin, VLA-1, is expressed by the majority of influenza-specifi
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
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.
39 alpha-chain of the type IV collagen receptor VLA-1, and these cells were highly activated, producing
42 These novel findings together indicate that VLA-1 is critically involved in the processes of lymphan
44 data demonstrated, for the first time, that VLA-1 blockade significantly suppressed corneal lymphang
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