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1 act epithelial cells express a wide range of B7 molecules.
2 of CTLA-4 can also function independently of B7 molecules.
3 purified CD8+ cells, even in the absence of B7 molecules.
4 ) mice with mice lacking B7-1, B7-2, or both B7 molecules.
5 assuming the absence of trans-stimulation by B7 molecules.
6 action of CD28 or CTLA-4 on the T cells with B7 molecules.
7 g CTLA-4, the inhibitory T cell receptor for B7 molecules.
8 ized in mouse strains lacking either or both B7 molecules.
9 press MHC class II proteins or costimulatory B7 molecules and fail to induce proliferation of T cells
10 blood monocytes (which express low levels of B7 molecules and FcgammaRs) compared with control mAb, b
11 umbilical vein endothelial cells (which lack B7 molecules and FcgammaRs) or by blood monocytes (which
13 The effect of ribavirin on the expression of B7 molecules and on CHS responses was neutralized by IL-
14 llows each CTLA-4 dimer to bind two bivalent B7 molecules and suggests that a periodic arrangement of
15 ase, but essentially unaltered expression of B7 molecules and T cell cytokine transcripts (interleuki
16 The intragraft transcript expression of the B7 molecules and their counterreceptors was defined usin
17 provides an important tool for examining how B7 molecules and their effects on CTLA-4 modulate T cell
19 e immune responses requires costimulation by B7 molecules, and Ag recognition without B7 is thought t
20 lls, were less dependent on costimulation by B7 molecules, and independent of costimulation by CD40.
23 er than PBAMCs, which use both the LFA-3 and B7 molecules, at costimulating IL-2 and IL-4 production.
24 mice that lack expression of the endogenous B7 molecules (B7 double knock-out mice), because of the
25 A comparison of the level of expression of B7 molecules by APC and CD4 T cells, under different con
26 o determine whether Ts inhibit expression of B7 molecules by blocking transcription, we cloned and ch
28 g stimulation of T cells, the recognition of B7 molecules by the CD28 costimulatory receptor increase
30 ets, we investigated the contribution of the B7 molecules CD80 and CD86 to the Th2 cytokine profile a
31 iltrating neutrophils sharply upregulate the B7 molecules CD80 and CD86, but they do not express CD40
32 nized homeostatic role for the costimulatory B7 molecules (CD80 and CD86) in preventing adipose infla
33 own to mediate costimulation, including CD28/B7 molecules (CD80 and CD86), CD40/CD40 ligand (CD40L, C
34 owed macrophage, recipient MHC class II, and B7 molecule co-localization by immunohistochemistry to G
38 h peak induction of HLA-DR and costimulatory B7 molecule (especially CD86) expression on B cells.
41 Our results indicate that MRP-14 regulates B7 molecule expression and reduces antigen presentation
42 a deficiency in costimulation due to lack of B7 molecule expression does not fully explain the inabil
46 o residues 75-84 of the alpha1 domain of HLA-B7 molecule (HLA-B7.75-84 [Allotrap]) inhibits cytotoxic
47 r both B7 molecules to determine the role of B7 molecules in activation of primary alloreactive CTL.
51 s in the presence of strong costimulation by B7 molecules in vitro and can reduce T cell-mediated ski
53 s, while B7-1 appeared to be the predominant B7 molecule involved in the ability of LT (E112K) to aug
54 indicates that B7-2 represents the dominant B7 molecule involved in the generation of an immune resp
55 These studies revealed that blockade of both B7 molecules is required for decreased production of IFN
56 in proteins share sequence homology with the B7 molecules, it is unclear whether they have any functi
59 e induced by blocking the interaction of the B7 molecule on the surface of antigen-presenting cells w
60 of co-stimulatory molecules on T cells with B7 molecules on antigen presenting cells plays an import
61 T cells is critical for the upregulation of B7 molecules on antigen-presenting B cells that subseque
62 in which activation-induced up-regulation of B7 molecules on APC leads to increased CD28 signaling an
64 o mouse heterotopic cardiac transplantation, B7 molecules on recipient cells rather than donor cells
66 ion of CTLA4Ig, a fusion protein which binds B7 molecules on the surface of antigen-presenting cells,
71 d to determine whether costimulation through B7 molecules plays any role in the unusual form of splen
73 a 10-amino-acid peptide derived from the HLA-B7 molecule, prolongs rat heterotopic cardiac allograft
76 T cell response that requires recognition of B7 molecules, since blocking B7 maintains T cells in an
77 uced the IgG2a response in mice lacking both B7 molecules, suggesting that CD4(-) cells may supply he
78 ity requires induction of tumor cell-encoded B7 molecules that are mediated by the cytoplasmic region
79 i differentially associates with variant HLA-B7 molecules that have peptide-binding groove mutations,
81 piratory tract epithelial cells up-regulates B7 molecules that regulate memory immune responses and t
82 made genetically deficient in either or both B7 molecules to determine the role of B7 molecules in ac
83 om neonatally induced T cell anergy requires B7 molecules to serve double functions, namely, costimul
86 tor (pHEBo) containing cDNA encoding the HLA-B7 molecule was transfected into lymphoblastoid cell lin
88 tion by naive T cells is highly dependent on B7 molecules, whereas IL-4 production by previously acti
89 Blocking the interaction of the CD28 and B7 molecules with a CTLA4Ig fusion protein abrogates the
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