ライフサイエンスコーパス: PD-L1

1 iver HSCs express programmed death ligand 1 (PD-L1).

2 we find that CMTM6 displays specificity for PD-L1.

3 her levels of inhibitory molecules IL-T3 and PD-L1.

4 CD8(+) T cells is dependent on TGF-beta and PD-L1.

5 expression of PD-L1 correlated strongly with PD-L1 (0.90), moderately with CD4 and CD8A, and weakly w

6 e microenvironment, including galectin-1 and PD-L1/2.

7 Thus, for tumor cell assessment of PD-L1, 3 of the 4 tests are concordant and reproducible

8 th dMMR or MSI expressed the CD274 molecule (PD-L1, 8/9) than PDACs without dMMR or MSI (4/10) (P = .

9 d expression of the immunosuppressive ligand PD-L1, a higher constitutive secretion of IL-6 and incre

10 pathway inhibitor significantly enhanced the PD-L1 Ab effect in enhancing NK cell cytotoxicity to cis

11 nized central role for MUC1-C in integrating PD-L1 activation with suppression of immune effectors an

12 ave evaluated the tumor targeting of an anti-PD-L1 adnectin after (18)F-fluorine labeling.

13 PD-L1 also potently suppressed nociceptive neuron excita

14 Lately, the anti-PD-L1 and -PD-1 immune therapies have become an importan

15 a human Ig-G1 monoclonal antibody targeting PD-L1 and approved in the USA for the treatment of metas

16 bits PD-L1 and programmed death-1 (PD-1) and PD-L1 and B7-1 interactions, reinvigorating anticancer i

17 recovered the known immune evasion molecules PD-L1 and CD47, and confirmed that defects in interferon

18 latory pathways and checkpoints such as PD-1/PD-L1 and CTLA-4.

19 However, the role of PD-L1 and PD-1 in regulating pain and neuronal function

20 ists, anti-CTLA4, or therapies targeting the PD-L1 and PD-1 pathway were excluded.

21 Expression of PD-1 and its ligands PD-L1 and PD-L2 in chronic rhinosinusitis with nasal pol

22 iptional inducer of the human genes encoding PD-L1 and PD-L2 through the vitamin D receptor, a ligand

23 Pembrolizumab prevents PD-1 ligation by both PD-L1 and PD-L2, preventing the immune dysregulation tha

24 1 and the associated PD-1 ligand loci, CD274/PD-L1 and PDCD1LG2/PD-L2, and copy number-dependent incr

25 Responses occurred across all PD-L1 and poor prognostic factor subgroups.

26 1 (PD-L1) monoclonal antibody that inhibits PD-L1 and programmed death-1 (PD-1) and PD-L1 and B7-1 i

27 Levels of the PD-L1 and VISTA inhibitory molecules increased on indepe

28 image analysis to examine the topography of PD-L1(+) and PD-1(+) cells in the tumor microenvironment

29 th protein 1/programmed death ligand 1 (PD-1/PD-L1) and cytotoxic T lymphocyte-associated protein 4 (

30 ells also express programmed death ligand 1 (PD-L1) and interleukin-10, and directly suppress liver c

31 teraction between Programmed Death Ligand 1 (PD-L1) and its receptor, PD-1, is an effective method of

32 s expressing programmed cell death ligand 1 (PD-L1) and report here on the interim analysis of the ma

33 xpressed high levels of MHC-I, low levels of PD-L1, and contained within their stroma CD8(+) T cells

34 xpressed low levels of MHC-I, high levels of PD-L1, and contained within their stroma regulatory T ce

35 s or upregulated that of HLA class I, B7-H3, PD-L1, and PD-L2, molecules that might limit NK cell fun

36 l proliferation, and the expression of CD25, PD-L1, and SLAM.

37 The tests use 4 separate PD-L1 antibodies on 2 separate staining platforms and ha

38 ith immuno-oncology drugs, including PD-1 or PD-L1 antibodies, OX40 ligand, or GITR ligand fusion pro

39 The combination of cGAMP and PD-L1 antibody exerted stronger antitumor effects than d

40 Reversing immune exhaustion with an anti-PD-L1 antibody may improve human immunodeficiency virus

41 To examine whether PD-L1 antibody reagents are interchangeable by quantitat

42 oral injection of Delta-24-RGDOX and an anti-PD-L1 antibody showed synergistic inhibition of gliomas

43 DCs when used alone or in combination with a PD-L1 antibody, confirming a role for T cells in antitum

44 Avelumab, a human monoclonal anti-PD-L1 antibody, has shown promising antitumour activity

45 measured by PET-CT with a radiolabeled anti-PD-L1 antibody.

46 tezolizumab (anti-programmed death-ligand 1 [PD-L1]) as treatment for metastatic urothelial cancer in

47 d for PD-L1 maturation but co-localizes with PD-L1 at the plasma membrane and in recycling endosomes,

48 ckpoint inhibitors (ICIs) targeting the PD-1/PD-L1 axis induce sustained clinical responses in a siza

49 blocking agents, such as anti-PD-1 and anti-PD-L1, because it was assumed that their antitumor immun

50 We have radiolabeled the PD-L1-binding Affibody molecule NOTA-ZPD-L1_1 with (18)F

51 cific T cells and T-cell activation via PD-1/PD-L1 blockade are currently being explored.

52 clinical response rate and efficacy of PD-1-PD-L1 blockade in patients with cancer.

53 in metastasis, a combination of MSC-oHSV and PD-L1 blockade increases IFNgamma-producing CD8(+) tumor

54 l kinase zeta (DGKzeta) with or without PD-1/PD-L1 blockade.

55 mmed death 1/programmed death ligand 1 (PD-1/PD-L1) blockade, have improved the treatment of non-smal

56 ction in a manner that was abrogated by anti-PD-L1 blocking antibody.

57 helper-dependent Ad (HDAd) that expresses a PD-L1 blocking mini-antibody (mini-body; HDPDL1) as a st

58 The predominant and high expression of PD-L1 by CD11b(+)F4/80(-)I-A(-) glomerular macrophages i

59 of CD4+ T cells leads to the upregulation of PD-L1 by recipient tissues and donor CD8+ T cells.

60 Thus, both tumor- and host-derived PD-L1 can play critical roles in immunosuppression.

61 sion and angiogenesis, diminished numbers of PD-L1(+) cancer cells, increased numbers of CD3(+) T cel

62 Panel 1 included pancytokeratin (AE1/AE3), PD-L1, CD4, CD8, CD3, CD68, and DAPI, and Panel 2 includ

63 d intra- and interbiopsy variability of PD1, PD-L1, CD8A, and CD4 mRNAs and their relationship with t

64 The dual therapy reduces PD-L1(+) cells and facilitates non-redundant tumour infi

65 Tumor-infiltrating PD-L1(+) cells isolated from tumor-bearing mice also exe

66 and support clinical investigations of PD-1/PD-L1 checkpoint blockade in anal SCC, irrespective of p

67 der such conditions is dependent on the PD-1/PD-L1 coinhibitory pathway.

68 inhibitory ligand programmed death ligand-1 (PD-L1) concurrent with enrichment of the programmed deat

69 eted MC38 cells in vivo, demonstrating tumor PD-L1 confers a selective advantage.

70 us brasiliensis Our results identify a novel PD-L1-controlled mechanism for type 2 polarization, with

71 IHC expression of PD-L1 correlated strongly with PD-L1 (0.90), moderately

72 Blockade of PD-L1/CTLA4 signaling dampened activation of SMX-NO-spec

73 ore, the treatment reduces the virus-induced PD-L1(+) DC, MDSC, TAM and Treg, as well as co-inhibitor

74 oimmune responses and the reduction of BO in PD-L1-deficient recipients suggest a potential therapeut

75 s in SPOP compromise ubiquitination-mediated PD-L1 degradation, leading to increased PD-L1 levels and

76 Wild-type MC38 cells outcompeted PD-L1-deleted MC38 cells in vivo, demonstrating tumor PD

77 Current methods of PD-L1 diagnosis have shown to vary based on the antibody

78 PD-L1 dictates the balance between Treg and IFN-gamma re

79 s in the open "face-back" tunnel through the PD-L1 dimer.

80 Results:(111)In-DTPA-anti-PD-L1 (dissociation constant, 0.6 +/- 0.1 nM) demonstrat

81 ly express the checkpoint inhibitor molecule PD-L1 during type 2 pulmonary responses.

82 epithelial cells with surface expression of PD-L1, E-cadherin, CD24, and VEGFR2 rapidly formed tumor

83 45 reversed the observed enhancement of anti-PD-L1 efficacy due to off-target suppression of the acti

84 commercially available, genetically defined PD-L1 engineered cell line array with a range of control

85 CL13(+) perivascular and CXCL12(+)LTB(+) and PD-L1(+) epithelial cells supporting TLS formation.

86 fied a peptide, RK-10, and used it to detect PD-L1 expressing tumors with immunohistochemistry or flo

87 resent a new first-line standard of care for PD-L1-expressing, advanced NSCLC.

88 mittee in all treated patients and by tumour PD-L1 expression (>/=5% and >/=1%).

89 Randomisation was stratified by PD-L1 expression (expression on <1% [IC0] or 1% to <5% [

90 1 expression and heterogeneity evaluation of PD-L1 expression across tumors in the same subject.

91 an effective method for obtaining tissue for PD-L1 expression analysis.

92 g may enable real-time follow-up of changing PD-L1 expression and heterogeneity evaluation of PD-L1 e

93 assessed in prespecified subgroups based on PD-L1 expression and in all patients.

94 1) expression levels in several cancers, but PD-L1 expression and its clinical significance in basal

95 ings reveal the involvement of DSB repair in PD-L1 expression and provide mechanistic insight into ho

96 le-domain antibody (anti-PD-L1 VHH) to track PD-L1 expression by immuno-positron emission tomography

97 2 concentrations, leading to upregulation of PD-L1 expression by recipient tissues and donor CD8+ T c

98 DC-PD-L1 expression correlated inversely with clinical dise

99 Immune cell PD-L1 expression correlated with increasing intensity of

100 Patients were required to have at least 1% PD-L1 expression detected on the tumour cells or in tumo

101 6192 bound to tumor tissues as a function of PD-L1 expression determined by immunohistochemistry.

102 stress, but the involvement of DSB repair in PD-L1 expression has not been investigated.

103 degree or composition of IC infiltration or PD-L1 expression in anal SCC.

104 PD-L1 expression in both the host and tumour compartment

105 er, with a significantly lower mean score of PD-L1 expression in both tumor and immune cells (tumor c

106 attract T cells into the tumour, and induce PD-L1 expression in cancer and immune cells, leading to

107 However, the underlying mechanisms of PD-L1 expression in cancer are not fully understood.

108 ranscriptional regulatory mechanisms control PD-L1 expression in cancer, it remains unknown whether s

109 Here we studied PD-L1 expression in human dermal lymphatic endothelial c

110 th (18)F-BMS-986192 are under way to measure PD-L1 expression in human tumors.

111 In vivo PET imaging clearly visualized PD-L1 expression in mice implanted with PD-L1(+), L2987

112 ls, and 94.9% (131 of 138) were positive for PD-L1 expression in TILs, defined as greater than 5% pos

113 UC1 subunit MUC1-C is sufficient to suppress PD-L1 expression in TNBC cells.

114 To assess PD-L1 expression in treatment-naive and treated BCCs.

115 an outlier that detected significantly less PD-L1 expression in tumor cells and immune cells.

116 oncordance between pathologists' scoring for PD-L1 expression in tumor cells ranged from ICCs of 0.83

117 odies to quantify interassay variability for PD-L1 expression in tumor cells showed high concordance

118 years), 89.9% (124 of 138) were positive for PD-L1 expression in tumor cells, and 94.9% (131 of 138)

119 tically significant reduction in labeling of PD-L1 expression in tumor cells.

120 1/PGE2 pathway involved in the regulation of PD-L1 expression in tumor-infiltrating myeloid cells and

121 8)F to yield a PET radioligand for assessing PD-L1 expression in vivo.

122 TA-HACA-PD1 most accurately visualized human PD-L1 expression in vivo.

123 ion and provide mechanistic insight into how PD-L1 expression is regulated after DSBs.

124 We also show the marked protective effect of PD-L1 expression on HCV-infected hepatoma cells against

125 tolytic and antiviral effects was blunted by PD-L1 expression on HCV-infected Huh7.5A2 cells, resulti

126 Patient selection was not based on PD-L1 expression or expression of other biomarkers, incl

127 ed non-small-cell lung cancer, regardless of PD-L1 expression or histology, with a favourable safety

128 th adaptive (IC-associated) and constitutive PD-L1 expression patterns were observed.

129 Patients unselected for PD-L1 expression received avelumab (10 mg/kg, 1 h intrav

130 atinum-based chemotherapy and unselected for PD-L1 expression received avelumab 10 mg/kg intravenousl

131 ell-intrinsic signaling in the regulation of PD-L1 expression remains unclear.

132 enic RAS signaling can upregulate tumor cell PD-L1 expression through a mechanism involving increases

133 meaningful clinical benefit, irrespective of PD-L1 expression, and was associated with an acceptable

134 should be used alone; if the patient has low PD-L1 expression, clinicians should offer standard chemo

135 ezolizumab; if tumor has negative or unknown PD-L1 expression, clinicians should use nivolumab or ate

136 oint therapy, if NSCLC tumor is positive for PD-L1 expression, clinicians should use single-agent niv

137 d tumor-infiltrating lymphocytes (TILs) with PD-L1 expression, intensities of expression, and associa

138 age, 51 [9.9] years) demonstrated tumor cell PD-L1 expression, regardless of HIV status.

139 emonstrate that RAS can drive cell-intrinsic PD-L1 expression, thus presenting therapeutic opportunit

140 (miRNAs) that have the potential to suppress PD-L1 expression.

141 or be negative (DeltamPD-L1 CT26) for human PD-L1 expression.

142 a and TNF-alpha synergistically up-regulated PD-L1 expression.

143 dehydrogenase (15-PGDH), resulted in reduced PD-L1 expression.

144 ed to understand the molecular regulation of PD-L1 expression.

145 ls, likely via suppression of lactate-driven PD-L1 expression.

146 Response to therapy was independent of PD-L1 expression.

147 s on the basis of programmed death ligand 1 (PD-L1) expression and human papillomavirus (HPV) status.

148 ritical driver of programmed death ligand-1 (PD-L1) expression in cancer and host cells, and baseline

149 n associated with programmed death ligand 1 (PD-L1) expression levels in several cancers, but PD-L1 e

150 ssion mediated by programmed death-ligand 1 (PD-L1) expression on cancer cells accompanied with virot

151 Here we show that programmed death ligand 1 (PD-L1) expression on tumor cells can render human CAR T

152 patient has high programmed death ligand 1 (PD-L1) expression, pembrolizumab should be used alone; i

153 A PD-L1-expression cutoff of 10% was associated with a hig

154 survival in the intention-to-treat (ITT) and PD-L1-expression population TC1/2/3 or IC1/2/3 (>/=1% PD

155 ntly longer with atezolizumab in the ITT and PD-L1-expression populations.

156 nd in recycling endosomes, where it prevents PD-L1 from being targeted for lysosome-mediated degradat

157 ession by MAPK/NF-kB-dependent activation of PD-L1 gene expression.

158 contrast to other transplant models in which PD-L1 generally shows protective functions, we demonstra

159 eath 1/programmed cell death 1 ligand 1 (PD1/PD-L1) generates durable therapeutic responses in a sign

160 s protective functions, we demonstrated that PD-L1 has divergent effects depending on its location in

161 d cell death protein 1 (PD-1) and its ligand PD-L1, have been approved for treating human cancers wit

162 icacy may be in part related to an effect on PD-L1(hi) B cells and Tfh cells.

163 ibitor molecule located at the center of the PD-L1 homodimer, filling a deep hydrophobic channel-like

164 fully human anti-programmed death-ligand 1 (PD-L1) IgG1 antibody, in patients with refractory metast

165 ith tumor-infiltrating lymphocytes (TIL) and PD-L1 IHC expression.

166 Although mutation load and PD-L1 immune cell (IC) staining have been associated wit

167 on treatment with CDK4/6 inhibitors and PD-1-PD-L1 immune checkpoint blockade to enhance therapeutic

168 Blockade of the PD-1/PD-L1 immune checkpoint pathway with monoclonal antibodi

169 ng inefficiency of the immunoprotective PD-1/PD-L1 immune checkpoint.

170 endently confirmed and compared with that of PD-L1 immunohistochemistry in 96 patients with head and

171 leading to more susceptible targets for anti-PD-L1 immunotherapy.

172 how that the coreceptor PD-1 with its ligand PD-L1, immunotherapy targets that inhibit T cell signali

173 ockade of STAT3 signaling downregulated PD-1/PD-L1 in a Tgfbr1/Pten 2cKO HNSCC mouse model.

174 er tumor cells promoted strong expression of PD-L1 in bone marrow-derived myeloid cells.

175 timulated transcription of the gene encoding PD-L1 in epithelial and myeloid cells, whereas the gene

176 treatment induces cell-surface expression of PD-L1 in epithelial and myeloid cells.

177 nt cells that can identify the expression of PD-L1 in malignant cells and macrophages, and different

178 the signals responsible for upregulation of PD-L1 in NSCLC cells and whether they are integrated wit

179 revealed a trend for increased expression of PD-L1 in responding patients and longer PFS with increas

180 ial therapeutic role of selectively blocking PD-L1 in the recipient.

181 ligands can be effective at targeting tumor PD-L1 in vivo, with good specificity and rapid clearance

182 ptor 2 (TLR2) and programmed death-ligand 1 (PD-L1) in regulating alpha-(1,3)-glucan-mediated DC acti

183 7) by quantitative immunofluorescence in the PD-L1 index tissue microarray.

184 human IgG1 monoclonal antibody that binds to PD-L1, inhibiting its binding to PD-1, which inactivates

185 ion could be partially overcome in vitro via PD-L1 inhibition and in a mouse model of STAT3 loss-of-f

186 The X-ray structures of the PD-L1/inhibitor complexes reveal one inhibitor molecule

187 The first chemical PD-1/PD-L1 inhibitors have been recently disclosed by Bristol

188 Development of small-molecule PD-1/PD-L1 inhibitors that could overcome these drawbacks is

189 uding those targeting CTLA-4/B7 and the PD-1/PD-L1 inhibitory pathways, are now available for clinica

190 iting the programmed death receptor 1 (PD-1)/PD-L1 interaction to enhance T cell-mediated immune func

191 espond to compounds that target the PD-1 and PD-L1 interaction, and the underlying mechanism(s) is no

192 apoptosis, thereby preventing GVHD, whereas PD-L1 interactions with CD80 in lymphoid tissue promoted

193 Programmed death ligand-1 (PD-L1) interacts with programmed death-1 (PD-1) and the

194 Hence, up-regulation of PD-L1 is a correlate of, but not a requirement for, HSC

195 Here, the authors show that PD-L1 is expressed on brown adipocytes, does not change

196 ntitumor immunity and demonstrate that tumor PD-L1 is not just a marker of suppressed antitumor immun

197 The immunosuppressive protein PD-L1 is upregulated in many cancers and contributes to

198 Programmed cell death ligand 1 (PD-L1) is part of an immune checkpoint system that is es

199 of programmed death 1 (PD-1) and its ligand (PD-L1) is partially understood.

200 Programmed cell death ligand-1 (PD-L1) is typically produced by cancer cells and suppres

201 Expression of PD-1 and PD-L1/L2 was evaluated at the cellular and tissue levels

202 ized PD-L1 expression in mice implanted with PD-L1(+), L2987 xenograft tumors.

203 ated PD-L1 degradation, leading to increased PD-L1 levels and reduced numbers of tumour-infiltrating

204 dendritic cells (DC) from GCA patients were PD-L1(lo), whereas the majority of vasculitic T cells ex

205 GN and the inhibition of proteinuria by anti-PD-L1 mAb supported the pathogenic role of these macroph

206 CMTM6 is not required for PD-L1 maturation but co-localizes with PD-L1 at the plas

207 PD-L1 may be a potential therapeutic target in several g

208 This novel function of recipient PD-L1 may result from the high degree of T-cell activati

209 that programmed cell death protein ligand 1 (PD-L1)-mediated inhibition of activated PD-1(+) T lympho

210 These results indicate that the outcome of PD-L1-mediated signaling in CD8+ T cells depends on the

211 The success of therapies that disrupt PD-L1-mediated tumour tolerance has highlighted the need

212 hydrophobic channel-like pocket between two PD-L1 molecules.

213 s a humanised antiprogrammed death-ligand 1 (PD-L1) monoclonal antibody that inhibits PD-L1 and progr

214 n through a mechanism involving increases in PD-L1 mRNA stability via modulation of the AU-rich eleme

215 i-tumor immunity dependent on degradation of PD-L1 mRNA.

216 vo studies were performed in PD-L1-positive, PD-L1-negative, and mixed tumor-bearing severe combined

217 In patients with PD-L1 of 1% or greater, confirmed objective responses we

218 suppress antitumor immunity, as deletion of PD-L1 on highly immunogenic MC38 tumor cells allows effe

219 Conditional deletion of PD-L1 on ILC2s impaired early Th2 polarization and cytok

220 In contrast, PD-L1 on MC38 colorectal adenocarcinoma cells is suffici

221 PD-L1 on nontumor cells is critical for inhibiting antit

222 ression population TC1/2/3 or IC1/2/3 (>/=1% PD-L1 on tumour cells or tumour-infiltrating immune cell

223 on via engagement of its inhibitory ligands, PD-L1 or PD-L2, is of particular interest due to recent

224 ibodies to immune checkpoints (CTLA-4, PD-1, PD-L1), or dual combinations modestly extended survival

225 PD-1/PD-L1 overexpression was found to be significantly assoc

226 trating that the IFN-gamma/TNF-alpha/miR-155/PD-L1 pathway is not restricted to HDLECs.

227 n by alpha-(1,3)-glucan was dependent on the PD-L1 pathway that negatively regulated interferon-gamma

228 tein 1 (PD-1) and programmed death-ligand 1 (PD-L1) pathway play an important immunosuppressive role

229 ed death-1 (PD-1)-programmed death ligand-1 (PD-L1) pathway.

230 rcentage of HCV-infected cells, and the PD-1/PD-L1 pathways and has antiviral and cytotoxic effects.I

231 -ligand 1 expression on tumor cells and ICs, PD-L1 patterns (adaptive vs constitutive), degree of IC

232 siceps-infected mice, demonstrating that the PD-L1(+)/PD-L2(+) subpopulation of AAMvarphis originates

233 e transfer of Ly6C(+) monocytes gave rise to PD-L1(+)/PD-L2(+), but not PD-L1(+)/PD-L2(-) cells in T.

234 ytes gave rise to PD-L1(+)/PD-L2(+), but not PD-L1(+)/PD-L2(-) cells in T. crassiceps-infected mice,

235 els aiming to characterize the expression of PD-L1, PD-1, and subsets of tumor associated immune cell

236 stochemical analysis for immune checkpoints (PD-L1, PD-1, LAG-3) and immune cell (IC) subsets (CD3, C

237 death protein 1 (PD-1) and the PD-1 ligands (PD-L1, PD-L2) is essential for malignant Hodgkin Reed-St

238 Expression of PD-1, PD-L1, PD-L2, TGF-beta, IL-5, and IL-10 mRNA was measure

239 mune function, yet the effectiveness of anti-PD-L1/PD-1 agents in enhancing natural killer (NK) cell'

240 sitivity to therapeutic agents targeting the PD-L1/PD-1 axis.

241 To compare the performance of 4 PD-L1 platforms, including 2 FDA-cleared assays, 1 test

242 r knowledge, this is the first reported anti-PD-L1 plus olaparib or cediranib combination therapy.

243 ogenic role of these macrophages but not the PD-L1(-) PMN in GN development and in inducing podocyte

244 The definition of PD-L1 positive lacks standardization, and prediction of

245 in patients with programmed death ligand 1 (PD-L1)-positive NSCLC.

246 ntaacetic acid (DTPA)-anti-PD-L1-to identify PD-L1-positive tumors in vivo.

247 In vivo studies were performed in PD-L1-positive, PD-L1-negative, and mixed tumor-bearing

248 PD-L1 positivity was defined as expression by immunohist

249 sis, upregulation of cytolytic activity, and PD-L1 positivity.

250 recruitment of MYC and NF-kappaB p65 to the PD-L1 promoter.

251 Here we show that PD-L1 protein abundance is regulated by cyclin D-CDK4 an

252 rstand the mechanistic pathways that control PD-L1 protein expression and stability, which can offer

253 nd CDK6 (hereafter CDK4/6) in vivo increases PD-L1 protein levels by impeding cyclin D-CDK4-mediated

254 s a novel molecular mechanism for regulating PD-L1 protein stability by a cell cycle kinase and revea

255 antitatively comparing the expression of the PD-L1 protein.

256 T3 signaling plays an important role in PD-1/PD-L1 regulation and the antitumor immune response of HN

257 At 24 h, the PD-L1-rich spleen and lungs demonstrated decreasing upta

258 in a nonhuman primate showed binding in the PD-L1-rich spleen, with rapid blood clearance through th

259 PET-CT imaging shows a robust and specific PD-L1 signal in brown adipose tissue (BAT).

260 PD-L1 signaling is not required for engraftment of embry

261 ne or in combination with inhibition of PD-1/PD-L1 signaling, in the treatment of MM and other B cell

262 Binding in the PD-L1(+) spleen was reduced by coadministration of BMS-9

263 el adjusting for age, sex, and BCC location, PD-L1 staining intensity in tumor cells increased with t

264 tained diffusely for PD-L2 and showed sparse PD-L1 staining.

265 A same-day PET imaging agent for measuring PD-L1 status in primary and metastatic lesions could be

266 the feasibility of noninvasively imaging the PD-L1 status of tumors by small-animal PET studies.

267 ssessment of programmed cell death ligand-1 (PD-L1) status.

268 totoxicity as a key mechanism by which tumor PD-L1 suppresses antitumor immunity and demonstrate that

269 showed that targeting MUC1-C associated with PD-L1 suppression, increases in tumor-infiltrating CD8(+

270 Recently, we developed an antibody-based PD-L1-targeted SPECT agent-(111)In-diethylenetriaminepen

271 domised phase 3 study to report results of a PD-L1-targeted therapy, with atezolizumab treatment resu

272 Clinical efficacy of PD-1/PD-L1 targeting relies upon the reactivation of tumor-sp

273 including dorsal root ganglion (DRG) produce PD-L1 that can potently inhibit acute and chronic pain.

274 This suggests that PD-1-PD-L1 therapies may also function through a direct effec

275 nse to anti-programmed cell death 1 and anti-PD-L1 therapies.

276 ical observation of HR during anti-PD-1/anti-PD-L1 therapy for LC, proved by comparing old pictures p

277 e marker in patients receiving anti-PD1/anti-PD-L1 therapy for LC.

278 dverse event occurring during anti-PD-1/anti-PD-L1 therapy for LC.

279 ctive tumor control upon treatment with anti-PD-L1 therapy.

280 nd anti-programmed cell death ligand 1 (anti-PD-L1 ) therapy for treatment of lung cancer (LC), in op

281 Strategies to block PD-L1, TIM3, and LAG3 might be developed for treatment o

282 mmunotherapeutic approaches that target PD-1-PD-L1 to enhance protective immune responses to A. fumig

283 (FDA) detect programmed cell death ligand 1 (PD-L1) to enrich for patient response to anti-programmed

284 ethylenetriaminepentaacetic acid (DTPA)-anti-PD-L1-to identify PD-L1-positive tumors in vivo.

285 igations showed that MUC1-C acted to elevate PD-L1 transcription by recruitment of MYC and NF-kappaB

286 Anti-PD-L1 treatment of tumor-bearing mice results in cessati

287 ntify patients who will best respond to anti-PD-L1 treatment while potentially providing key informat

288 of 14 patients with HR after anti-PD-1/anti-PD-L1 treatment, recruited between September and Decembe

289 untreated stage IV or recurrent NSCLC and a PD-L1 tumor-expression level of 1% or more to receive ni

290 elect HIV-positive and HIV-negative cases in PD-L1+ tumor areas associated with ICs.

291 mor cells in vitro and enhanced clearance of PD-L1+ tumor xenografts in vivo.

292 ongly inhibited phosphorylation of STAT1 and PD-L1 up-regulation, suggesting that diminished SOCS3 ex

293 hat Ku70/80 depletion substantially enhances PD-L1 upregulation after X-rays.

294 gests that exogenous cellular stress induces PD-L1 upregulation in cancer.

295 labeled camelid single-domain antibody (anti-PD-L1 VHH) to track PD-L1 expression by immuno-positron

296 xicity when neutralizing antibody of PD-1 or PD-L1 was added.

297 Tumor-induced expression of PD-L1 was limited to F4/80(+) macrophages and Ly-6C(+) m

298 To refine detection of PD-L1, we have identified a peptide, RK-10, and used it

299 ression of T-cell checkpoint signals such as PD-L1, which may inhibit their functionality against sol

300 Importantly, combining antibody against PD-L1 with antibodies against TIM3, LAG3, or CTLA4 furth

301 Interaction of PD-L1 with PD-1 in GVHD-targeted tissues resulted in CD8