ライフサイエンスコーパス: co-stimulatory

1 derived from the CD19-BBz prototype bearing co-stimulatory 4-1BB and CD3zeta domains.

2 Therefore, B7RP-1 exhibits co-stimulatory activities in vitro and in vivo.

3 LIGHT has potent, CD28-independent co-stimulatory activity leading to T-cell growth and sec

4 mmunological synapse where it can exert both co-stimulatory and co-inhibitory functions.

5 isease-dependent manner, induce differential co-stimulatory and co-inhibitory molecule expression, an

6 CCR7(+) DCs expressed both co-stimulatory and co-inhibitory molecules, which may un

7 self-antigens involves a complex network of co-stimulatory and co-inhibitory molecules.

8 In this review, we will focus on the role of co-stimulatory and co-inhibitory pathways in two systemi

9 major component of which is a large array of co-stimulatory and co-inhibitory pathways that modulate

10 critically impacted by the constellation of co-stimulatory and co-inhibitory receptors expressed on

11 these superfamilies but potentially between co-stimulatory and co-inhibitory receptors.

12 revealed coexpression of multiple additional co-stimulatory and co-inhibitory receptors.

13 linical development of agents targeting both co-stimulatory and co-inhibitory T cell receptors.

14 Signals transmitted by T cell, co-stimulatory and cytokine receptors control Thp lineag

15 T cells, T-cell-receptor ligation-along with co-stimulatory and cytokine signals-induces a glycolytic

16 ll receptor and is modulated by signals from co-stimulatory and inhibitory molecules as well as by mi

17 function and the dynamic integration of the co-stimulatory and T-cell receptor signals are just begi

18 re we report an optimization strategy of the co-stimulatory and targeting properties of a FGFR4 CAR.

19 anti-CD19 CAR (CAR19) comprised of the 4-1BB co-stimulatory and TNFRSF19 transmembrane domains, showi

20 The co-stimulatory antigen CD28 has been shown to bind to se

21 lted from CTLA-4-dependent downregulation of co-stimulatory B7-family proteins on cDCs, mediated by T

22 We present the state of the art in co-stimulatory blockade approaches, including rational c

23 of high-dose bone marrow transplantation and co-stimulatory blockade can thus achieve allogeneic bone

24 Co-stimulatory blockade has been shown to prolong allogr

25 als conditioned with anti-CD4, anti-CD8, and co-stimulatory blockade in addition to lethal irradiatio

26 transfusion (DST) can synergize with T cell co-stimulatory blockade in inducing tolerance in several

27 ction and Tg graft loss following CD40:CD40L co-stimulatory blockade in this model provides opportuni

28 een shown to overcome tolerance induction by co-stimulatory blockade or regulatory T cells.

29 -alpha responses and impaired the ability of co-stimulatory blockade to extend allograft survival.

30 alpha in the graft recipient synergized with co-stimulatory blockade to induce tolerance.

31 Unexpectedly, though, co-stimulatory blockade with anti-CD154 or CTLA4-Ig indu

32 ects and with tolerogenic potential, such as co-stimulatory blockade, would be a great improvement if

33 Abatacept, a co-stimulatory blocker, and rituximab, a B cell depletin

34 re driven by the scaffold's incorporation of co-stimulatory bound ligands and soluble molecules, and

35 cell antigen receptor and, thus, function as co-stimulatory, but not direct stimulatory, molecules.

36 Here, we show that the co-stimulatory cell-surface molecule LFA-1 requires magn

37 e cells, and gene-engineering with synthetic co-stimulatory circuits.

38 e crystal structure of the human CTLA-4/B7-1 co-stimulatory complex at 3.0 A resolution.

39 s are amplified by coligation of BCR and the co-stimulatory complex, and several self Ags targeted in

40 amplification of STAT3 phosphorylation under co-stimulatory conditions.

41 tion pathway can impact greatly not only the co-stimulatory context in which the antigen is presented

42 8 transmembrane domain upstream of the 4-1BB co-stimulatory domain as a driver of potent anti-tumor a

43 ile of multi-targeted dual CARTs favored the co-stimulatory domain linked to the binder of the more r

44 s independent of the CAR construct's design, co-stimulatory domain, and tumor model.

45 release and despite the absence of an extra co-stimulatory domain.

46 R and the other BiCisCAR with the same 4-1BB co-stimulatory domain.

47 rative engineering of transmembrane (TM) and co-stimulatory domains plus overexpression of c-Jun lowe

48 xtensive clinical use, the attributes of CAR co-stimulatory domains that impact persistence and resis

49 oth FGFR4 and CD276, containing two distinct co-stimulatory domains, have superior prolonged persiste

50 CAR construct design, including co-stimulatory domains, hinge, transmembrane regions, pr

51 Here is reported a co-stimulatory effect of angiotensin II (AngII) by showi

52 B7-1 is one of the co-stimulatory factors which plays an important role in

53 gs support a substantially revised model for co-stimulatory function in the primary GC response, with

54 acking isoforms, which may down-regulate the co-stimulatory function of dectin-1.

55 containing 2 (TMIGD2), a recently discovered co-stimulatory immune receptor, is aberrantly expressed

56 T cells and macrophages can be altered with co-stimulatory inhibitors, but may not be a significant

57 -4, is an important mediator of adhesive and co-stimulatory interactions that govern cutaneous immune

58 cytokines but partially dependent on direct co-stimulatory interactions via ICOSL-ICOS.

59 rapeutic interventions targeting ICOS.ICOS-L co-stimulatory interactions.

60 around the concept that CD86 is the initial co-stimulatory ligand based on its more abundant and ear

61 fy that cancer cell expression of the T-cell co-stimulatory ligand CD80 sensitizes murine tumors to a

62 Recent studies identified ICAM-1 as a co-stimulatory ligand that binds to lymphocyte function

63 nflammatory mediator release is modulated by co-stimulatory ligands (CD80 and CD86) expressed by the

64 a CD40-CD40L interactions, cDC1s provide key co-stimulatory ligands and cytokines to mount and sustai

65 umor phenotypes, p53-dependent expression of co-stimulatory ligands, and proliferation of co-cultured

66 ed from cancer cells engineered to express a co-stimulatory marker.

67 Neither cell population was positive for the co-stimulatory markers CD40, CD80 and CD86, but both dem

68 promoted BMDC maturation and upregulation of co-stimulatory markers, including CD40, CD86, and MHC-II

69 regulation of immunity relevant cytokine and co-stimulatory markers.

70 ic cell (DC) lines using cellular activation co-stimulatory/maturation markers.

71 In particular, targeting co-stimulatory members of the tumor necrosis factor rece

72 drugs in development are those targeting the co-stimulatory modulation, cytokines and the B and T cel

73 Interactions between inducible co-stimulatory molecule (ICOS) and ICOS-ligand (ICOS-L)

74 The inducible co-stimulatory molecule (ICOS) is a CD28 homologue impli

75 The inducible co-stimulatory molecule (ICOS), a third member of the CD

76 y (Treg) cells with high levels of inducible co-stimulatory molecule (ICOS).

77 CD80 is a co-stimulatory molecule and plays a leading role in T ce

78 ation of MHC class I and II antigens and the co-stimulatory molecule B7 suggests increased immunogeni

79 6 and IL-8, as well as the expression of the co-stimulatory molecule B7.1, which is required for the

80 eD-dependent depletion of surface MHCII, the co-stimulatory molecule B7.2, and suppression of T cell

81 face receptor Slamf1 functions not only as a co-stimulatory molecule but also as a microbial sensor o

82 The co-stimulatory molecule CD28 is essential for activation

83 on signals delivered through the TCR and the co-stimulatory molecule CD28.

84 N6; (2) the T cell antigen CD3; and (3) the co-stimulatory molecule CD28.

85 IL-36alpha increased the expression of the co-stimulatory molecule CD40 and enhanced the ability of

86 production, showed robust expression of the co-stimulatory molecule CD40L, and promoted the developm

87 the role of complement regulator and T cell co-stimulatory molecule CD46, and also discussed are cha

88 ed significantly higher MHC class II and the co-stimulatory molecule CD80 compared to Tetherin KO DCs

89 henotypically mature as they up-regulate the co-stimulatory molecule CD86 from intracellular storages

90 otein ligand (GITRL) is a recently described co-stimulatory molecule expressed by antigen-presenting

91 Co-stimulatory molecule expression (CD40, 80, 86, and I-

92 assessed by cytokine production (ELISA) and co-stimulatory molecule expression (flow cytometry).

93 We demonstrate that the increased co-stimulatory molecule expression (MHC II and CD86) and

94 uence immune cell communication by affecting co-stimulatory molecule expression and ENaC activity on

95 amma than human macrophages, as reflected by co-stimulatory molecule expression and TNF-alpha product

96 ment activation, neutrophil recruitment, and co-stimulatory molecule expression on dendritic cells ar

97 transplantation to study the role of MHC and co-stimulatory molecule expression on DST cells in media

98 no interleukin (IL)-12p35 mRNA, low surface co-stimulatory molecule expression, and CCR transcripts,

99 ntigen presentation through up-regulation of co-stimulatory molecule expression, and promote survival

100 Loss of Nrf2 results in increased co-stimulatory molecule expression, enhanced T cell stim

101 n (PSA) and containing transgenes for T-cell co-stimulatory molecule expression, including CD80.

102 ficantly inhibit BMDC maturation by reducing co-stimulatory molecule expression.

103 allele diminishes the expression of CD40, a co-stimulatory molecule for T cell polarization.

104 tein ligand (GITRL), a ligand for the T cell co-stimulatory molecule GITR, is expressed by keratinocy

105 To investigate the roles of B7-1 and/or B7-2 co-stimulatory molecule in the development of graft arte

106 The clustering state of the co-stimulatory molecule lymphocyte function-associated a

107 CD27 is a co-stimulatory molecule of T cells, and inherited CD27 d

108 up-regulated the expression of the negative co-stimulatory molecule PD-L1, and this can be prevented

109 Our studies thus define a previously unknown co-stimulatory molecule that may be involved in the nega

110 , detected by NLDC-145 antibody and the CD80 co-stimulatory molecule, as well as Ia antigen on exposu

111 The co-stimulatory molecule, CD86, which is critical for DC/

112 h its cellular receptor 1 (HAVCR1), a T-cell co-stimulatory molecule, inhibits the function of Treg c

113 lpha4beta1 (CD49d) which, as well as being a co-stimulatory molecule, is required for CLL cells to un

114 press GITRL, and that through this important co-stimulatory molecule, they have the potential to infl

115 In this context, signals deriving from co-stimulatory molecules (i.e., CD80, CD86), co-inhibito

116 s major histocompatibility complex (MHC) and co-stimulatory molecules and are recognized and killed b

117 ed into chemokine-producing DCs that express co-stimulatory molecules and can prime naive T cells.

118 Signals from T-cell receptors, co-stimulatory molecules and cytokine receptors direct t

119 immune response depends on the expression of co-stimulatory molecules and cytokines by antigen-presen

120 y, the improved understanding of the role of co-stimulatory molecules and cytokines IL-10 and IL-2 in

121 rrelation, DCs up-regulate the expression of co-stimulatory molecules and cytokines.

122 nterleukin (IL)-1beta signaling that induces co-stimulatory molecules and IL-21, which enable mouse a

123 ILC3s was necessary and sufficient to reduce co-stimulatory molecules and increase PD-L1 bioavailabil

124 um induced significant surface expression of co-stimulatory molecules and maturation markers in a mur

125 intrinsic effect leading to up-regulation of co-stimulatory molecules and subsequent T cell activatio

126 uble molecules, and depended on the types of co-stimulatory molecules and the context in which they w

127 10, which in turn can downregulate important co-stimulatory molecules and the cytokines IL-12 and IFN

128 rd, activation of TLRs induces expression of co-stimulatory molecules and the release of cytokines th

129 ibodies and fusion proteins targeting T-cell co-stimulatory molecules are now in late-stage clinical

130 quire surface expression of MHC class II and co-stimulatory molecules as well as T-cell stimulatory a

131 The induction of CTL effectors requires co-stimulatory molecules B7-1 and/or B7-2 on host antige

132 MHC-II+ macrophages and cells expressing the co-stimulatory molecules B7-2 and CD40, as well as IgM +

133 cells, we investigated the expression of the co-stimulatory molecules BB-1, B7-1 (CD80) B7-2 (CD86) a

134 s (migDC2) that similarly upregulate surface co-stimulatory molecules but express pathogen-specific c

135 ation of integrins and blunted expression of co-stimulatory molecules by overactivating the NFAT (nuc

136 5(+) cells with reduced up-regulation of the co-stimulatory molecules CD80, CD86, and CD68.

137 rated in the genetic absence of the negative co-stimulatory molecules CTLA-4 and PD-1.

138 Blocking CD28, CD154 (CD40L), or both co-stimulatory molecules has been efficacious in prevent

139 potently induced expression of cytokines and co-stimulatory molecules HLA-DR and CD86 in human newbor

140 recently strengthened by the upregulation of co-stimulatory molecules ICOS/ICOS-L and PD-L1.

141 Here, we review the targeting of co-stimulatory molecules in autoimmune diseases, focusin

142 n terms of up-regulation of MHC class II and co-stimulatory molecules in the absence and presence of

143 gs indicate distinct roles for B7-1 and B7-2 co-stimulatory molecules in the development of GAD, pote

144 ocytosis is downregulated, the expression of co-stimulatory molecules is enhanced, and newly formed i

145 ajor histocompatibility complex class II and co-stimulatory molecules on antigen-presenting cells (AP

146 The interaction of co-stimulatory molecules on T cells with B7 molecules on

147 We also analyzed expression of different co-stimulatory molecules on virus-specific CD8+ and fork

148 expressed significantly higher levels of the co-stimulatory molecules OX40 (37.2% of FOXP3+ cell popu

149 The co-stimulatory molecules SLAMF3 and SLAMF6 have been imp

150 activation downstream of the TCR as well as co-stimulatory molecules such as CD28.

151 n several pathways of regulation of ILC2s by co-stimulatory molecules such as ICOS, regulatory T cell

152 Therefore, we hypothesized that co-stimulatory molecules that preferentially bind CD28 o

153 equires signals from the T cell receptor and co-stimulatory molecules to license effector functions o

154 f interaction, examples include adhesion and co-stimulatory molecules which confirm physical interact

155 he allograft response, and blocking positive co-stimulatory molecules with active delivery of inhibit

156 in a multi-step process involving cytokines, co-stimulatory molecules, and a variety of antigen-prese

157 ires signals from the T cell receptor (TCR), co-stimulatory molecules, and cytokines.

158 ules, including the T-cell receptor complex, co-stimulatory molecules, and integrins unrelated to LFA

159 s to attenuate T cell activation via TCR and co-stimulatory molecules, and its reduction during T cel

160 s, regulation of MHC expression, activity of co-stimulatory molecules, and the signalling cascades ac

161 t sizes, the use of adjuvants, cytokines and co-stimulatory molecules, epitope enhancement and the st

162 ich are members of the extended B7 family of co-stimulatory molecules, have diverse functions in the

163 ity in function, which is not seen for other co-stimulatory molecules, is responsible for the unique

164 ption factors, c-Maf and NFIL3, and negative co-stimulatory molecules, LAG-3, TIGIT, PD-1 and TIM-3,

165 ure and process antigens, express lymphocyte co-stimulatory molecules, migrate to lymphoid organs and

166 during viral infections, by manipulation of co-stimulatory molecules, or in the development of tumor

167 associated with higher expression levels of co-stimulatory molecules, PD-L1, IL-6, TNF-alpha, and IL

168 synapse', including integrins, cadherins and co-stimulatory molecules, reveal in detail the molecular

169 ed with lipopolysaccharide do not upregulate co-stimulatory molecules, secrete greatly diminished amo

170 In contrast to wild-type CD80, the evolved co-stimulatory molecules, termed CD28-binding protein (C

171 on of relevant peptide epitopes, addition of co-stimulatory molecules, the development of novel vehic

172 class II family, cytokines, chemokines, and co-stimulatory molecules, was significantly altered in t

173 s is associated with increased expression of co-stimulatory molecules.

174 igh expression of PD-L1 and PD-L2 as well as co-stimulatory molecules.

175 sion of major histocompatibility complex and co-stimulatory molecules.

176 wn to engage intraepithelial T cells through co-stimulatory molecules.

177 f dendritic cell (DC) maturation markers and co-stimulatory molecules.

178 tory cytokines, as well as adhesion cell and co-stimulatory molecules.

179 -inducible expression of CD40, CD80 and CD86 co-stimulatory molecules.

180 ajor histocompatibility complex antigens and co-stimulatory molecules.

181 ivation and immune function are regulated by co-stimulatory molecules.

182 istocompatibility complex (MHC) class II and co-stimulatory molecules.

183 mune responses by differential expression of co-stimulatory molecules.

184 ) and MLN expressing MHC-II but little or no co-stimulatory molecules.

185 le vaccines together with antibodies against co-stimulatory molecules.

186 vels of major histocompatibility complex and co-stimulatory molecules.

187 n of IRF4, antigen processing components and co-stimulatory molecules.

188 Activated DCs expressed high levels of co-stimulatory molecules; released inflammatory cytokine

189 the MHC; they are structurally related to B7-co-stimulatory molecules; they are functionally implicat

190 o express a modified FceR1gamma with a 4-1BB co-stimulatory motif.

191 of B lymphocytes, dysregulated cytokine and co-stimulatory networks, infection with potentially onco

192 with RCC, including ICIs with novel targets, co-stimulatory pathway agonists, modified cytokines, met

193 studies identify a previously unknown T-cell co-stimulatory pathway as a potential therapeutic target

194 with CD28 and constitute an essential T-cell co-stimulatory pathway in the initiation of antigen-spec

195 CD40-CD154 (CD40 ligand) interaction in the co-stimulatory pathway is involved in many (auto)immune

196 The CD28 co-stimulatory pathway is well established for T cell ac

197 Here, we demonstrate that the CD28 co-stimulatory pathway regulates the trafficking of self

198 LS mouse model, we identified a role for the co-stimulatory pathway, a key regulator of immune respon

199 ce to study the impact of targeting a T cell-co-stimulatory pathway, and demonstrate that targeting T

200 l activation, but it remains unclear whether co-stimulatory pathways also control T cell differentiat

201 approaches for targeting B-cell subsets and co-stimulatory pathways are described here in detail.

202 cal CD28 and the non-canonical SLAMF3/SLAMF6 co-stimulatory pathways cooperate in the recruitment of

203 and that crosstalk between co-inhibitory and co-stimulatory pathways in pathogen-specific CD4 T cells

204 ocyte activation can be targeted by blocking co-stimulatory pathways or inhibiting major histocompati

205 Using either agents that block co-stimulatory pathways or the immunosuppressive drug ra

206 e decreasing FVIII uptake by APCs, modifying co-stimulatory pathways, inducing regulatory T-cell prod

207 -/- mice suggest the existence of additional co-stimulatory pathways.

208 ), in the presence of B7- and CD40-dependent co-stimulatory pathways.

209 lternatively with therapies targeting T-cell co-stimulatory pathways.

210 ith the desensitization of the TRAF1-binding co-stimulatory receptor 4-1BB, 4-1BBL-deficient mice hav

211 ning, we identified an immune cell-specific, co-stimulatory receptor B7.2 (CD86) as a co-receptor of

212 Interestingly, targeting the co-stimulatory receptor CD137 with an agonistic antibody

213 immunoglobulin and ITIM domain (TIGIT), the co-stimulatory receptor CD226 and their ligand PVR are a

214 TIGIT and CD96 together with the co-stimulatory receptor CD226 form a pathway that is ana

215 n-presenting cells (APCs), activate the main co-stimulatory receptor CD28 on T cells in trans.

216 l factors such as CD80 and CD86, ligands for co-stimulatory receptor CD28, and interleukin 2 are requ

217 d the ability of CD80 to activate the T cell co-stimulatory receptor CD28.

218 n species (ROS), in a manner mediated by the co-stimulatory receptor CD40.

219 OX40 is a co-stimulatory receptor expressed on activated T cells.

220 ) iDCs have lower basal GSH levels, enhanced co-stimulatory receptor expression, impaired phagocytic

221 ies and to regulate pathways that control DC co-stimulatory receptor expression.

222 sis and has been implicated in modulating DC co-stimulatory receptor expression.

223 Co-stimulatory receptor gene expression is regulated by

224 ulfide modification can be translated to the co-stimulatory receptor h4-1BB, another member of the tu

225 e depends on continued signaling through the co-stimulatory receptor ICOS (inducible co-stimulator).

226 Conversely, expression of the complementary co-stimulatory receptor of TIGIT, CD226 (DNAM-1) was sig

227 CD137 (4-1BB) is a co-stimulatory receptor on immune cells and Nectin-4 is

228 lymphocyte activation molecule (Slamf)1 is a co-stimulatory receptor on T cells and regulates cytokin

229 (CTX) and an agonist antibody targeting the co-stimulatory receptor OX40 (OX86) provides potent anti

230 d rodents exhibit atypical expression of the co-stimulatory receptor OX40 on CD4 T cells and that the

231 cal inhibitors, we demonstrate that enhanced co-stimulatory receptor phenotype of Nrf2(-/-) iDC does

232 V and HIV-1 Nefs down-modulate CD28, a major co-stimulatory receptor that mediates effective T-cell a

233 CD28, a major co-stimulatory receptor, is responsible for the optimal

234 was also suggested that TIM3 might act as a co-stimulatory receptor.

235 ytokine production suggests NTB-A is a novel co-stimulatory receptor.

236 eceptors is counterbalanced by expression of co-stimulatory receptors and it is only SIRPalpha(+) cel

237 ing cascades that integrate information from co-stimulatory receptors and locally available cytokines

238 nts targeting additional immune checkpoints, co-stimulatory receptors and/or co-inhibitory receptors

239 Immature DCs (iDCs) expressing low levels of co-stimulatory receptors are highly efficient at antigen

240 es of the cytoplasmic tails of integrins and co-stimulatory receptors in complex with intracellular s

241 imulation of the T cell receptor complex and co-stimulatory receptors is associated with acute tyrosi

242 ranscription factor NF-kappaB to antigen and co-stimulatory receptors is required for the temporal co

243 Modulation of co-inhibitory and co-stimulatory receptors of the immune system has become

244 pression of cytolytic effector molecules and co-stimulatory receptors such as 4-1BB.

245 e identify that targeting alternative T-cell co-stimulatory receptors, in particular OX-40 and 4-1BB

246 es to study signaling mechanisms in the TCR, co-stimulatory receptors, synthetic signaling molecules

247 munity, upregulates the expression of T-cell co-stimulatory receptors, with the inducible co-stimulat

248 ling pathways through antibodies that target co-stimulatory receptors.

249 of the T cell receptor (TCR) zeta chain and co-stimulatory receptors.

250 zes recent progress on different features of co-stimulatory regulation and chemokine-mediated homing

251 d in the T-cell receptor signal strength and co-stimulatory requirements needed for their generation.

252 , and concurrently promotes the reception of co-stimulatory rescue signals by supporting B cell migra

253 cells are cycling but are defective in their co-stimulatory response when stimulated.

254 Given the co-stimulatory role of natural-killer group 2, member D

255 (CARs) targeting GD2 but without an embedded co-stimulatory sequence (first-generation CARs).

256 Here we evaluated selective blockade of the co-stimulatory signal (CD28-B7) with Lulizumab, which pr

257 d thus far produce either an activation or a co-stimulatory signal alone, thus limiting the spectrum

258 TNFSF4 produces a potent co-stimulatory signal for activated CD4+ T cells after e

259 ICOSLG encodes a co-stimulatory signal for T-cell proliferation and cytok

260 sponse to antigenic challenge by providing a co-stimulatory signal for TCR.

261 t increased levels of cFLIP(L), along with a co-stimulatory signal from Toll-like receptor 3, activat

262 To be fully active, immune T cells need a co-stimulatory signal in addition to the main antigen-dr

263 lexes (ICs) in human CD4(+) T-cells produced co-stimulatory signal like CD28 that triggered IFN-gamma

264 The co-stimulatory signal promotes T-cell proliferation, lym

265 B7-2 on antigen-presenting cells deliver the co-stimulatory signal through CD28 and CTLA-4 on T cells

266 4(+) T-cells phosphorylate Syk and provide a co-stimulatory signal to CD4(+) T-cells in the absence o

267 cell activation receptor that can provide a co-stimulatory signal to other activation receptors and

268 er338 through PI 3-kinase and Pak provides a co-stimulatory signal which together with Ras leads to s

269 ells is tightly regulated by a combinational co-stimulatory signal, and dominance of negative co-stim

270 onses require both an antigen-specific and a co-stimulatory signal.

271 ire an antigen-specific signal and a second, co-stimulatory, signal for optimal T-cell activation.

272 hways suggested LGMD2B-specific increases in co-stimulatory signaling between dendritic cells and T c

273 t EGFRvIII demonstrates a reliance on PDGFRA co-stimulatory signaling during the tumorigenic process

274 sing on the role of antigen presentation and co-stimulatory signaling pathways in cancer immunology.

275 ch to this problem is to manipulate specific co-stimulatory signaling pathways to enhance CD8(+) effe

276 in sIBM there is upregulation of ICOS.ICOS-L co-stimulatory signalling in association with enhanced p

277 keletal engagement, which is permissive, and co-stimulatory signals (calcium or protein kinase C) gen

278 et, which are dependent on the antigen dose, co-stimulatory signals and the cytokine environment, cri

279 in human cells, promoting the expression of co-stimulatory signals and the secretion of pro-inflamma

280 Because co-stimulatory signals are critical for regulating T-cel

281 tical framework for clinical trials in which co-stimulatory signals are manipulated in an attempt to

282 ction in mice, suggesting that other in vivo co-stimulatory signals can overcome the requirement of B

283 cells are dependent on accessory cell-bound co-stimulatory signals for activation.

284 The OX40-OX40L pathway provides crucial co-stimulatory signals for CD4 T cell responses, however

285 f the TNFR family known to provide essential co-stimulatory signals for T cell growth and B cell Ig s

286 eceptor 4-1BB and its ligand 4-1BBL provides co-stimulatory signals for T-cell activation and prolife

287 es the pre-TCR, beta-selection also requires co-stimulatory signals from Notch receptors - key cell f

288 ctivation by NFAT without the cooperation of co-stimulatory signals in lymphocytes can also impose a

289 nced network of positive and negative T-cell co-stimulatory signals is important in regulating T-cell

290 TLR-inducible expression of co-stimulatory signals is one of the mechanisms of self/

291 ating T-cell activation, an understanding of co-stimulatory signals may enable the design of rational

292 ar and can present antigen in the context of co-stimulatory signals required for the stimulation of b

293 r whether or how the inducible expression of co-stimulatory signals would distinguish between self an

294 ative signals concurrent with blocking CD154 co-stimulatory signals would facilitate islet allograft

295 was enhanced by concurrent blockade of CD154 co-stimulatory signals, as demonstrated by T-cell prolif

296 Co-stimulatory signals, cytokines and transcription fact

297 Here, we propose that the integration of co-stimulatory signals, which regulate the ability of pr

298 and(s) on T cells, thereby delivering T cell co-stimulatory signals.

299 TNF-alpha and suppressing the expression of co-stimulatory surface markers CD80 and CD86.

300 T-cell receptor (TCR) and the CD28 and 4-1BB co-stimulatory surface molecules.