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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.
19                 Here we have shown that CD28 co-stimulation, an extracellular cue intrinsically requi
20 and receptors play important roles in T-cell co-stimulation and co-inhibition.
21 uced expected patterns of T-cell activation, co-stimulation and co-inhibition.
22 l activation, that is, antigen presentation, co-stimulation and cytokine milieu.
23 t from antigen recognition in the absence of co-stimulation and inflammation, and is associated with
24                          Abatacept modulates co-stimulation and prevents full T-cell activation.
25 inhibiting regulatory cells, boosting T-cell co-stimulation and using combinations of recombinant cyt
26                                    Excessive co-stimulation and/or insufficient co-inhibition can lea
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
29 er, the transcriptional consequences of CD28 co-stimulation are not completely understood.
30 g cells (APC) which are capable of providing co-stimulation as well.
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
33                Treatment with rapamycin plus co-stimulation blockade resulted in massive apoptosis of
34                                              Co-stimulation blockade with abatacept (CTLA4-Ig) will s
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
40 nfusion, chimerism, T cell depletion, and/or co-stimulation blockade.
41                                 Studies of a co-stimulation blocker (abatacept), tumor necrosis facto
42               Belatacept is a first-in-class co-stimulation blocker in development for primary mainte
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.
45                                    Moreover, co-stimulation by CXCL12 together with soluble VCAM-1 po
46 3 ligation alone, activation of JNK requires co-stimulation by the CD28 receptor.
47 nt findings, however, suggest that eliciting co-stimulation can also induce tolerance.
48 diac allograft survival with combined T cell co-stimulation (CD28-CD80/86 and CD154-CD40) blockade in
49                             TGF-beta and TCR co-stimulation converts thymic CD4+CD25+ T cells into CD
50 duration of antigenic stimulation, degree of co-stimulation, cytokine environment, and CD4(+) T-cell
51                                       T-cell co-stimulation delivered by the molecules B7-1 or B7-2 t
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
54                                 Furthermore, co-stimulation enhanced production of CCL2 as well as ph
55                               CB1R and IL-6R co-stimulation enhanced the differentiation of rat corti
56 g expression of optimal surrogate markers of co-stimulation/exhaustion signatures in independent data
57 ity LFA-1, only high affinity LFA-1 provides co-stimulation for CD8(+) T cell activation.
58 evels of co-stimulation, with RA attenuating co-stimulation from interfering from FoxP3 induction.
59                                Historically, co-stimulation has been regarded as a prerequisite for T
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
66           We demonstrate here that CD27-CD70 co-stimulation in the thymus rescues developing Treg cel
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
71                             TCR ligation and co-stimulation induce cellular division; however, optima
72 mmune activation while suppression of T-cell co-stimulation is coincident with selective upregulation
73                                     Although co-stimulation is essential for boosting and shaping the
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
77       Adoptive T-cell therapy using CD3/CD28 co-stimulation likely requires in vivo generation of ant
78           Our findings demonstrate that GITR co-stimulation mediates antitumor immunity by promoting
79                                              Co-stimulation modulation with abatacept slowed reductio
80                                The selective co-stimulation modulator abatacept demonstrated efficacy
81           Upon antigen engagement and proper co-stimulation, naive lymphocytes exit quiescence and un
82 on, production of pathogenic antibodies, and co-stimulation of autoreactive T cells.
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
85                  These data demonstrate that co-stimulation of G(12/13) and G(i) pathways is sufficie
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
88      In addition, TxA2 generation induced by co-stimulation of Gi and Gz pathways, which is dependent
89              This effect is specific for the co-stimulation of IGFBP-3 with TGF-beta1 because a combi
90 ssion of IL-13Ralpha1 is more dependent upon co-stimulation of immunoglobulin and CD40 receptors.
91 ng is analogous to the activation of ICat by co-stimulation of M2 and M3 receptors.
92 pression is regulated, we considered whether co-stimulation of NIH3T3 cells with RA and epidermal gro
93                                 In addition, co-stimulation of purified human T cells was significant
94 ting dendritic cells (DC) and is involved in co-stimulation of T cells by DC.
95      CD97 has been shown recently to mediate co-stimulation of T cells via CD55.
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
98                                      Whereas co-stimulation of the T-cell antigen receptor (TCR) and
99             In both, most fields elicited by co-stimulation of two laser beams were well explained by
100                            As the CD154-CD40 co-stimulation pathway provides essential second signal
101                    These include blockade of co-stimulation pathways and agonism of coinhibitory path
102          Its biologic effects include T-cell co-stimulation, promotion of erythropoiesis, angiogenesi
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
105         The consequence is a decrease in the co-stimulation required to develop an effective immune r
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
108                                    A lack of co-stimulation results in peripheral T-cell tolerance, w
109 by antigen/MHC (signal 1) and CD28-dependent co-stimulation (signal 2), resting CD4(+) T cells commit
110                                     Negative co-stimulation signaling by hepatic T-cells might be dev
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
113                                     However, co-stimulation studies show that Galphaq receptor agonis
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
116                                     CD3/CD28 co-stimulation, therefore, generates T1 or T2 population
117  encounter foreign antigen along with proper co-stimulation they undergo rapid and extensive clonal e
118                 The effects of B7-1 and B7-2 co-stimulation through CD28 depend on the strength of th
119                                    Augmented co-stimulation through NKG2D confers a high rate of surv
120                We demonstrate that augmented co-stimulation through NKG2D during priming paradoxicall
121    These findings demonstrate that augmented co-stimulation through NKG2D is effective in rescuing CD
122                   T-cell activation requires co-stimulation through receptors such as CD28 and antige
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
127                                              Co-stimulation via FcepsilonRI, using IgE/antigen, and C
128                                              Co-stimulation via the CD28 receptor is required for eff
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
132 fects of SIL, yet this was not restorable by co-stimulation with ANP.
133 ial cells exhibited synergistic responses to co-stimulation with AP and lipopolysaccharide.
134                                              Co-stimulation with ATP and either PTHrP (43-52) or PTHr
135                                              Co-stimulation with both MCP-1 and IL-6 did not elevate
136 1-mediated transcriptional activity, whereas co-stimulation with both Wnt3a and BMP-2 markedly reduce
137                                              Co-stimulation with carbachol and 8-pCPT-2'-O-Me-cAMP le
138                                              Co-stimulation with CRH and AVP results in complex patte
139                                              Co-stimulation with CRH and AVP results in complex patte
140                                              Co-stimulation with CSE, IL-17A and aeroallergens furthe
141                                              Co-stimulation with forskolin and acetylcholine promoted
142 tivation of AP-1:Luc observed in response to co-stimulation with growth factors and Ro-31-8220.
143                                         Upon co-stimulation with HCV-E2 and HIV-gp120, we observed a
144 on and function can be profoundly altered by co-stimulation with inhibitory receptors.
145                                              Co-stimulation with insulin does not affect the IL-1beta
146 ssive transcriptional activity of NFAT1 upon co-stimulation with ionomycin and phorbol 12-myristate 1
147                                              Co-stimulation with TGF-beta1 and TNF-alpha induced an a
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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