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1 CD2 superfamily, NTB-A, important in T cell co-stimulation.
2 tigen is encountered in the presence of full co-stimulation.
3 umor activity is further enhanced by in vivo co-stimulation.
4 ell activation, but does not account for all co-stimulation.
5 mounts, was required for the effect of B7-H1 co-stimulation.
6 tokines together with cell contact-dependent co-stimulation.
7 and whether the interaction plays a role in co-stimulation.
8 ntigen 4-Ig, which blocks B7-mediated T-cell co-stimulation.
9 s and involves both antigen presentation and co-stimulation.
10 inhibited JNK responsiveness during CD3/CD28 co-stimulation.
11 ve T cells and with reduced requirements for co-stimulation.
12 g stimuli and produce IL-2 in the absence of co-stimulation.
13 mour cells, and could be further enhanced by co-stimulation.
14 tive injury, antigen presentation and T cell co-stimulation.
15 ated antigen) is a critical event for T cell co-stimulation.
16 t antigen presenting cells or through direct co-stimulation.
17 roteins involved in antigen presentation and co-stimulation.
18 rials that are centered on modulating T-cell co-stimulation.
23 t from antigen recognition in the absence of co-stimulation and inflammation, and is associated with
25 inhibiting regulatory cells, boosting T-cell co-stimulation and using combinations of recombinant cyt
27 addition to CD4 T-cell activation and T-cell co-stimulation are critical components in the developmen
28 cell-receptor triggering and the delivery of co-stimulation are essential events leading to T cell ex
31 contrast, treatment with cyclosporine A and co-stimulation blockade abolished T-cell proliferation a
32 se CD154 monoclonal antibody (mAb) to induce co-stimulation blockade leads to long-term murine islet
35 h CD28-B7 and CD40-CD40 ligand interactions (co-stimulation blockade) inhibited proliferation of allo
36 These results indicate that in synergy with co-stimulation blockade, CXCR3 is a viable therapeutic t
37 rejection and tolerance induction following co-stimulation blockade, providing new targets for immun
38 promote allograft rejection particularly in co-stimulation blockade-based immunosuppressive regimens
39 tes memory T cells and, when combined with a co-stimulation blockade-based regimen using cytotoxic T
43 ory cytokines inhibit DC maturation, whereas co-stimulation-blocking agents can also promote the indu
44 ross-presentation of associated peptides and co-stimulation by APCs that interact with alpha(2)M.
48 diac allograft survival with combined T cell co-stimulation (CD28-CD80/86 and CD154-CD40) blockade in
50 duration of antigenic stimulation, degree of co-stimulation, cytokine environment, and CD4(+) T-cell
52 l type I interferons (IFNs) directly inhibit co-stimulation-dependent T reg cell activation and proli
53 ICOS-ligand (ICOS-L) are crucial for T-cell co-stimulation, effector cell differentiation and memory
56 g expression of optimal surrogate markers of co-stimulation/exhaustion signatures in independent data
58 evels of co-stimulation, with RA attenuating co-stimulation from interfering from FoxP3 induction.
60 6), anti-CD20 and those that modulate T-cell co-stimulation have consistently shown good efficacy in
61 pase 8 activation were not inhibited by IBOP co-stimulation, however, resulting in a 2.6-fold increas
62 f CTLA4Ig-induced blockade of CD28-B7 T-cell co-stimulation in conjunction with intrathymic immunomod
63 Much attention has focused on the role of co-stimulation in dictating tolerance versus immunity to
64 e roles of cytokines, antigenic signals, and co-stimulation in guiding T cell responses, data indicat
65 reinforces the key role of CD154-CD40 T-cell co-stimulation in the pathophysiology of liver I/R injur
67 en receptor-mediated death can be rescued by co-stimulation, in which the roles of protein kinase C a
68 ed IFN-gamma production; however, only MCP-1 co-stimulation increased IL-4 production, whereas MIP-1
69 educe Akt S473 phosphorylation and to reduce co-stimulation-independent IL-2 production in Dicer-defi
70 aggregation defects could be rescued by ADP co-stimulation, indicating that they are a consequence o
72 mmune activation while suppression of T-cell co-stimulation is coincident with selective upregulation
74 y, we find that where evidence of CD4 T-cell co-stimulation is pronounced, that of CD8 T-cell exhaust
75 xhausted' T-cell state driven by CD2-induced co-stimulation is reduced by signals through the exhaust
76 ell receptor (TCR) stimulation together with co-stimulation is sufficient for the activation of both
83 g G protein-coupled signaling profile, where co-stimulation of both receptors leads to strongly reduc
84 igger activation of natural killer cells and co-stimulation of effector T cells, and may thus promote
86 olishment of platelet aggregation induced by co-stimulation of G(q) and G(i) pathways, but not by G(1
87 nogen receptor antagonist was not rescued by co-stimulation of G12/13 pathways in the presence of Pyk
90 ssion of IL-13Ralpha1 is more dependent upon co-stimulation of immunoglobulin and CD40 receptors.
92 pression is regulated, we considered whether co-stimulation of NIH3T3 cells with RA and epidermal gro
96 wever, antibody stimulation was dependent on co-stimulation of the FcgammaII receptor (CD32) since sp
97 f a vaccine targeting PSA that also enhances co-stimulation of the immune system did not seem to exac
103 tivation of CD8(+) T cells in the absence of co-stimulation provided by CD80 and CD86 molecules.
104 l antigen receptors and specific CD2-induced co-stimulation provided to human CD8 T cells in vitro, s
106 es in the thymic medulla, in which CD27-CD70 co-stimulation rescues developing Treg cells from apopto
107 estern blot analysis showed that HU and IL-6 co-stimulation resulted in increased levels of Sp1 and S
109 by antigen/MHC (signal 1) and CD28-dependent co-stimulation (signal 2), resting CD4(+) T cells commit
111 nctions triggered by antigen recognition and co-stimulation signals are associated with a rapid and i
112 h LNCaP cells are capable of this mode of AR co-stimulation, stable expression of mutant beta-catenin
114 der certain levels of TCR signal strength or co-stimulation, such as effector/memory (CD4(+)TEM and C
115 that "peripheral" blockade of CD28-B7 T-cell co-stimulation synergizes with the "central" immunosuppr
117 encounter foreign antigen along with proper co-stimulation they undergo rapid and extensive clonal e
121 These findings demonstrate that augmented co-stimulation through NKG2D is effective in rescuing CD
123 to present tumor antigens in the context of co-stimulation to overcome tolerance and induce tumor-sp
124 amma upon antigenic stimulation, and require co-stimulation to proliferate to anti-CD3 stimulation.
125 a skewing of the TIGIT/CD226 axis from CD226 co-stimulation towards TIGIT-mediated inhibition of CD8(
126 ocytes, antigen recognition with appropriate co-stimulation triggers exit from G0 phase of the cell c
129 the master transcription factor Bcl-6, ICOS co-stimulation was essential to maintain the phenotype b
130 onstrate that CD8 T cells require DNAM-1 for co-stimulation when recognizing antigen presented by non
131 TLA-4 Ig and anti-CD40L antibody) that block co-stimulation, which is essential for full T cell activ
136 1-mediated transcriptional activity, whereas co-stimulation with both Wnt3a and BMP-2 markedly reduce
146 ssive transcriptional activity of NFAT1 upon co-stimulation with ionomycin and phorbol 12-myristate 1
148 ne expression in human mesangial cells after co-stimulation with thrombin and tumor necrosis factor a
149 a moderate upregulation of preproET-1 mRNA, co-stimulation with TNFalpha resulted in a strong and pr
150 romoter (-4.4 kbp to 204 bp) was overcome by co-stimulation with TNFalpha, providing a possible mecha
151 ccurs even in the presence of high levels of co-stimulation, with RA attenuating co-stimulation from
152 SCO-100/Matrix-M (AbISCO), to assess if TLR9 co-stimulation would quantitatively or qualitatively mod
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