ライフサイエンスコーパス: PD-L1

1 , one of which is programmed death-ligand 1 (PD-L1).

2 ssion of CD86 and programmed death ligand 1 (PD-L1).

3 ay have an impact on the prognostic power of PD-L1.

4 option for patients with high expression of PD-L1.

5 clinically relevant immune checkpoint, PD-1/PD-L1.

6 x and CRP influenced the prognostic power of PD-L1.

7 dendritic cells (DCs), which highly express PD-L1.

8 b, as well as a soluble antigen, circulating PD-L1.

9 pembrolizumab is an option for low positive PD-L1.

10 is an option in select cases of low positive PD-L1.

11 study reports a novel approach for targeting PD-L1.

12 cells endogenously expressing high levels of PD-L1.

13 rigenesis, even in the absence of endogenous PD-L1; (3) PD-L1(+) T cells engaged PD-1(+) macrophages,

14 "do not eat me" signal for macrophages) and PD-L1 (a T-cell inactivator) on their surface.

15 ting ENO1, alone or in combination with anti-PD-L1 Ab or ACY241, to restore anti-MM immunity, enhance

16 Combination of ENO1i and anti-PD-L1 Ab or HDAC6i ACY-241 enhances autologous MM-specif

17 Genetically or pharmacologically modulating PD-L1 acetylation blocks its nuclear translocation, repr

18 th exhaustion markers FoxP3(+), PD-1(+), and PD-L1(+) (all p <= 0.0001).

19 he efficacy and safety of atezolizumab (anti-PD-L1) alone and combined with bevacizumab (anti-VEGF) i

20 tions of 27.85-798.43 (amol/mug protein) for PD-L1 and 16.96-129.89 (amol/mug protein) for PD-1.

21 he determinants of response to combined PD-1/PD-L1 and angiogenic pathway inhibition and may aid in t

22 ne checkpoint inhibitors, which target PD-1, PD-L1 and CTLA-4, are increasingly used for certain canc

23 reveal new therapeutic targets beyond PD-1, PD-L1 and CTLA-4, as well as new combination approaches.

24 rtoire of sebocytes, notably by upregulating PD-L1 and IL10.

25 We discover that PD-L1 and JAK2 transcripts are negatively regulated by b

26 Except for one sample, PD-L1 and PD-1 in all samples were quantifiable using th

27 T-cells with cancer cells harboring genomic PD-L1 and PD-L2 amplification in the second.

28 BTICs expressed high constitutive levels of PD-L1 and PD-L2 and that PD-L2 overexpression inhibited

29 The PD-1 ligands PD-L1 and PD-L2 are commonly expressed on the surface of

30 e current and preceding studies confirm that PD-L1 and PD-L2 are expressed in a high percentage of OA

31 o identify that GATA2 is sufficient to drive PD-L1 and PD-L2 expression and is necessary for PD-L2 ex

32 he cell-intrinsic mechanisms of constitutive PD-L1 and PD-L2 expression in brain tumors.

33 mor sampling may influence interpretation of PD-L1 and PD-L2 expression in ocular adnexal tumors.

34 The degree of PD-L1 and PD-L2 expression was also associated with the

35 late expression of the PD-1 pathway ligands, PD-L1 and PD-L2, remain poorly understood.

36 identify a non-immune checkpoint function of PD-L1 and provide an unexpected concept that GSDMC/caspa

37 uss our claim that endogenous tumor exosomal PD-L1 and tumor-derived exosome-induced PD-L1 are two of

38 Dual blockade of PD-L1 and VEGF has enhanced anticancer immunity through

39 pting the PD-1/PD-L1 complex by antagonizing PD-L1 and, therefore, restores activation of T cells sim

40 Programmed death ligand-1 (PD-L1) and cluster of differentiation 80/86 (CD80/86) in

41 1 (PD-1), programmed cell death 1 ligand 1 (PD-L1) and cytotoxic T lymphocyte antigen 4 (CTLA-4) imm

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

43 staining for programmed cell death ligand 1 (PD-L1) and mismatch repair proteins MutL homolog 1 (MLH1

44 Programmed death ligand 1 (PD-L1) and PD-L2 are ligands for PD-1; the former is ubi

45 exhibit frequent copy-number gains of CD274 (PD-L1) and PDC1LG2 (PD-L2) on chromosome 9p24.1.

46 e by upregulating programmed death-ligand 1 (PD-L1) and resulted in tumor relapse.

47 protein 1 (PD-1), programmed death ligand 1 (PD-L1), and cytotoxic T lymphocyte-associated protein 4

48 subtypes express programmed death-ligand 1 (PD-L1), and natural killer (NK) cells are involved in tr

49 on of cells with elevated CD68, CD44, CD11c, PD-L1, and CD205 expression levels.

50 immune high group is enriched in higher CD3, PD-L1, and genomically-unstable molecular subtype, sugge

51 elated with protein abundance only for PD-1, PD-L1, and IDO1 and tumor mutation burden did not predic

52 ve the decreased expression of ICAM1, CD11b, PD-L1, and the reduced aggregation following the prolong

53 the nanotransformer-based vaccine with anti-PD-L1 antibodies results in over 83 days of survival and

54 ammed cell death ligand 1 (PD-L1) by an anti-PD-L1 antibody (avelumab) in combination with recombinan

55 Treatment with PD-L1 antibody also reduces Treg and Breg elevation in t

56 ption of CD274, which combined with the anti-PD-L1 antibody to reactivate T cells function for tumor

57 nation of EpAb2-6 with atezolizumab, an anti-PD-L1 antibody, almost completely eliminated tumors.

58 utic efficacy equivalent or superior to anti-PD-L1 antibody.

59 omal PD-L1 and tumor-derived exosome-induced PD-L1 are two of the most notable mechanisms of exosome-

60 ls with elevated expression of ICAM1, CD11b, PD-L1 as well as enhanced swarming and aggregation.

61 However, the newly characterized PD-L1:B7-1 ligand-ligand cis-interaction and its ability

62 ults suggest that the successful outcomes of PD-L1 based therapies in patients with PD-L1 negative tu

63 patients were masked to patient-level tumour PD-L1 biomarker results.

64 Type 1 conventional DCs are essential for PD-L1 blockade and they upregulate PD-L1 upon antigen up

65 bed as a new mechanism for the resistance to PD-L1 blockade therapy in multiple cancers, including PC

66 patients, especially those resistant to PD-1/PD-L1 blockade therapy.

67 ibitor dramatically enhanced the efficacy of PD-L1 blockade treatment in a syngeneic model of PCa by

68 ed the sensitivity of HR(+) 59-2-HI tumor to PD-L1 blockade, suggesting that antiprogestins may impro

69 ranslocation to enhance the efficacy of PD-1/PD-L1 blockade.

70 rocess and cut off the secretion of exosomal PD-L1 by blocking the transcription of CD274, which comb

71 blockade of programmed cell death ligand 1 (PD-L1) by an anti-PD-L1 antibody (avelumab) in combinati

72 Blockade of programmed death-ligand 1 (PD-L1) by therapeutic antibodies has shown to be a promi

73 radiation with a caspase inhibitor and anti-PD-L1 can effectively control tumors by sequentially blo

74 mmed death-1/programmed death-ligand 1 (PD-1/PD-L1) can effectively regulate the activity of T cells

75 point" receptors CTLA-4, PD-1, or its ligand PD-L1, can produce durable responses in some patients.

76 The clinical study of PD-L1 CAR haNKs is warranted.

77 PD-L1 CAR haNKs reduced levels of macrophages and other

78 The PD-L1 (CD274) immune-checkpoint ligand is often upregula

79 Combination with a PD-L1 checkpoint blockade further enhances inhibition of

80 s with PD-L1 negative tumors respond to PD-1/PD-L1 checkpoint inhibition remains unclear.

81 enhancing the therapeutic efficiency of anti-PD-L1 checkpoint inhibitors in vivo.

82 ve advanced cancer patient treated with PD-1/PD-L1 checkpoint inhibitors.

83 hat NK cells (haNKs) engineered to express a PD-L1 chimeric antigen receptor (CAR) haNKs killed a pan

84 l as well as treatment outcomes according to PD-L1 combined positive score (CPS).

85 e compound is capable of disrupting the PD-1/PD-L1 complex by antagonizing PD-L1 and, therefore, rest

86 0 months (2.7-3.9) for the anti-PD-1 or anti-PD-L1-containing groups.

87 ng programmed death-1 (PD-1) and its ligand (PD-L1) continue to show limited durable success in clini

88 There was no significant interaction between PD-L1 CPS >= 10 and treatment arm for progression-free s

89 PD-L1 CPS >=1 was detected in 95% of OASC, while PD-L1 T

90 urvival and overall survival assessed in the PD-L1 CPS of 10 or more, CPS of 1 or more, and intention

91 patients, which indicates a deregulated PD-1/PD-L1 cross-talk between these cells.

92 Moreover, PD-L1 deficiency leads to compromised expression of mult

93 cells at low effector-to-target ratios in a PD-L1-dependent fashion.

94 Treatment of xenograft tumors resulted in PD-L1-dependent tumor growth inhibition.

95 ment of syngeneic tumors resulted in CD8 and PD-L1-dependent tumor rejection or growth inhibition and

96 Only when PD-1 interacts with PD-L1 did the FSY react with a proximal histidine of PD-

97 lymph node, identifying a potential role for PD-L1 expressing dendritic cells within the lymph node i

98 lerated wound closure through recruitment of PD-L1-expressing myeloid cells to the wound site.

99 ccompanied by enhanced antitumor immunity in PD-L1-expressing triple-negative breast cancer and thus

100 nts had baseline tumor biopsies positive for PD-L1 expression (n = 28/40 evaluable), and response rat

101 oups in the population of patients with high PD-L1 expression (the high PD-L1 population) and between

102 For patients with high PD-L1 expression (TPS >= 50%) and SCC, the Expert Panel

103 transporter copper transporter 1 (CTR-1) and PD-L1 expression across many cancers but not in correspo

104 PD-L1-positive tumour types, suggesting that PD-L1 expression alone is not sufficient as a biomarker

105 subsets in peripheral blood as well as their PD-L1 expression and complex formation with T cells.

106 ion with interferon-gamma induced endogenous PD-L1 expression and restricted T cell activation and gr

107 alysis revealed a strong association between PD-L1 expression and that of NFKB2 and carbonic anhydras

108 We also observed that LXA4 treatment reduces PD-L1 expression and that PD-L1 expression is an importa

109 therapy (taxane or gemcitabine-carboplatin), PD-L1 expression at baseline (combined positive score [C

110 activity in brain metastases from NSCLC with PD-L1 expression at least 1% and is safe in selected pat

111 interaction, CD44 positively correlated with PD-L1 expression at the mRNA and protein levels in prima

112 eloped to noninvasively determine whole-body PD-L1 expression by PET.

113 or cells indeed grow out, which depends upon PD-L1 expression by wild-type cells.

114 ow that intratumoral copper levels influence PD-L1 expression in cancer cells.

115 Immunohistochemical staining of PD-L1 expression in meningiomas showed 43% positivity in

116 OSAS patients revealed an increased PD-1 and PD-L1 expression in T cells and monocytes, respectively,

117 In vitro IFNgamma treatment increased PD-L1 expression in the tumor cell lines and caused up t

118 PD-L1 expression in the tumor microenvironment significa

119 receptor CD44 as a key positive regulator of PD-L1 expression in these cancers.

120 treatment reduces PD-L1 expression and that PD-L1 expression is an important immune evasion strategy

121 PD-L1 expression is typically low or absent in SCLC, whi

122 observe higher ADORA1, lower ATF3, and lower PD-L1 expression levels in tumor tissues from nonrespond

123 IFN-alpha increased HLA-DR, CD80, CD86, and PD-L1 expression on healthy donor monocytes.

124 However, the regulation of PD-L1 expression on tumor cells is still poorly understo

125 interaction was not correlated with clinical PD-L1 expression scores in malignant melanoma.

126 a new mechanism of how cancer cells regulate PD-L1 expression through epigenetic factors and provides

127 Tumor interferon (IFN) signaling promotes PD-L1 expression to suppress T cell-mediated immunosurve

128 PD-L1 expression was not significantly associated with r

129 Tumor PD-L1 expression was positive in 119 (15.6%), with 17 (2

130 ell lines and 4T1 mouse mammary tumor cells, PD-L1 expression was regulated by the nuclear receptor N

131 We also show an association PD-L1 expression with NFKB2 expression and its induction

132 ith non-Hodgkin lymphoma; all responders had PD-L1 expression).

133 Tumor MCPyV status, PD-L1 expression, and tumor mutational burden (TMB) were

134 tive voice-response system and stratified by PD-L1 expression, choice of platinum, and smoking status

135 That work includes evaluation of tumour cell PD-L1 expression, gene expression signatures, CD8(+) T c

136 hare a high level of immune infiltration and PD-L1 expression, similar to basal tumors.

137 ocytes and increased HLA-DR, CD80, CD86, and PD-L1 expression.

138 frequent CDKN2A/B alterations, and increased PD-L1 expression.

139 as the factor transcriptionally upregulating PD-L1 expression.

140 ing both the intrinsic and IFN-gamma-induced PD-L1 expression.

141 ditions validated the association of CA9 and PD-L1 expression.

142 atients with high programmed death ligand 1 (PD-L1) expression (tumor proportion score [TPS] >= 50%)

143 osuppressive programmed cell death ligand-1 (PD-L1) expression by downregulating EGFR signaling.

144 Positive tumor programmed death ligand 1 (PD-L1) expression was defined as combined positive score

145 cell death protein 1 (PD-1), and its ligand (PD-L1) expression.

146 Drugs that block PD-1 or PD-L1 facilitate endogenous antitumor immunity and, beca

147 CD44 is a potential target to suppress PD-L1 function in TNBC.

148 h using the immune checkpoint inhibitor anti-PD-L1-gamma1 as an effector gene.

149 at early, self-activating expression of anti-PD-L1-gamma1 can overcome the immunosuppressive environm

150 imal germinal center (GC)-rich region of the PD-L1 gene promoter.

151 grammed cell death 1 (PD1) and PD1 ligand 1 (PD-L1) have had early success in the clinic, which has l

152 Nonetheless, PD-L1 IHC was positive in 93% of LELC cases.

153 For patients with PD-L1 immune cell-positive metastatic triple-negative br

154 ant that overall survival in the subgroup of PD-L1 immune cell-positive patients could only be formal

155 y overall survival analysis in patients with PD-L1 immune cell-positive tumours, median overall survi

156 on during programmed cell death protein 1 or PD-L1 immune checkpoint inhibition, further validation o

157 mining mechanisms of resistance to alphaPD-1/PD-L1 immune-checkpoint immunotherapy is key to developi

158 ll death 1 (PD-1):programmed death-ligand 1 (PD-L1) immune checkpoint pathway have ushered in the mod

159 E5 as a mediator of resistance to anti-PD-1/PD-L1 immunotherapy and demonstrates the antitumor activ

160 a novel mechanism of resistance to anti-PD-1/PD-L1 immunotherapy mediated by HPV E5, which can be exp

161 We found that T cell expression of PD-L1 in cancer was regulated by tumor antigen and steri

162 Blocking PD-L1 in established tumors promotes re-activation of tu

163 nd that Lmdd-MPFG promoted the expression of PD-L1 in HCC cells but resensitized the tumor local T ce

164 Here we show the clinical significance of PD-L1 in meningioma as a marker that can predict tumor r

165 al significance and regulatory mechanisms of PD-L1 in meningioma is not yet fully characterized.

166 malignancies, data on the prognostic role of PD-L1 in MPE is scarce.

167 PD-L2 abundance exceeded PD-L1 in over half the specimens and the drug target pro

168 r myeloid cells endogenously expressing high PD-L1 in peripheral blood from patients with head and ne

169 In addition to an endogenous role for PD-L1 in profibrotic TGFbeta signaling, TGFbeta stimulat

170 ownregulated cellular and membrane levels of PD-L1 in tumor cells by 50% as measured by Western blott

171 expression of the immunosuppressive protein PD-L1 in tumors.

172 nabling irreversible binding of PD-1 to only PD-L1 in vitro and in vivo.

173 primary source of programmed death-ligand 1 (PD-L1) in human and murine CCA.

174 including programmed cell death 1 ligand 1 (PD-L1), in a STING-dependent manner.

175 PD-L1 induced immune suppression has increasingly gained

176 The mechanisms by which PD-1/PD-L1 inhibition elicits anti-tumor immunity are not ful

177 r Cell, Dammeijer et al. address the role of PD-L1 inhibition specifically within the tumor-draining

178 ngineered oncolytic virus that coexpresses a PD-L1 inhibitor and GM-CSF.

179 t the oncolytic virus is able to secrete the PD-L1 inhibitor that systemically binds and inhibits PD-

180 designed a trial to test the activity of the PD-L1 inhibitor, atezolizumab, with carboplatin and nab-

181 ich patients benefit the most from anti-PD-1/PD-L1 inhibitors are unknown, making treatment-related d

182 ssess the efficacy and toxicity of anti-PD-1/PD-L1 inhibitors in advanced and metastatic cancer.

183 mTOR inhibitors, CTLA-4 inhibitors, or PD-1/PD-L1 inhibitors, etc.

184 using checkpoint inhibitors, such as PD-1 or PD-L1 inhibitors.

185 mall cell lung cancer, those with lower PD-1/PD-L1 interaction had significantly worsened survival.

186 The PD-1/PD-L1 interaction was not correlated with clinical PD-L1

187 mors selecting for an elevated level of PD-1/PD-L1 interaction, there is a greater dependence on this

188 intervention, we quantitatively imaged PD-1/PD-L1 interactions in tumor samples from patients, emplo

189 eta stimulated-human lung fibroblast-derived PD-L1 into extracellular vesicles (EVs) capable of inhib

190 PD-L1 is expressed in tumor cells and its interaction wi

191 Silencing INCR1 decreases the expression of PD-L1, JAK2, and several other IFNgamma-stimulated genes

192 Furthermore, PD-L1 knockdown decreased the TGFbeta-dependent inductio

193 onal tumor mutation burden (TMB), as well as PD-L1 level.

194 Part 2 characterized changes in PD-L1 levels and CD8(+) cells following treatment (prima

195 umetinib lowered cellular, but not membrane, PD-L1 levels of tumors, and consequently, no treatment-i

196 r, this deletion induces the upregulation of PD-L1 levels, which inactivates cocultured T cells in vi

197 Conventional treatment with an anti-PD-L1 mAb had no significant antitumor effect, indicatin

198 interactions of exhausted CD8 + T-cells and PD-L1 + macrophages and PD-L1 + tumor cells as mechanist

199 l clustering of exhausted CD8 + T-cells with PD-L1 + macrophages in the first, and exhausted CD8 + T-

200 y respond to immunotherapies due to elevated PD-L1(+) macrophages.See related article by Arnesen et a

201 injection with the oncolytic virus overcomes PD-L1-mediated immunosuppression during both the priming

202 t IL-12-primed T cells are resistant to PD-1/PD-L1-mediated suppression and retain effector function.

203 racer can discriminate a range of tumor cell PD-L1 membrane expression levels.

204 t proteins of the programmed-death ligand 1 (PD-L1) microenvironment in live lymphocytes and selectiv

205 s) were associated with longer OS under anti-PD-L1 monotherapy as compared to chemotherapy, reflectin

206 Ipilimumab (anti-CTLA-4) or anti-PD-1/PD-L1 monotherapy failed to show a significant benefit.

207 platin-ineligible patients who received anti-PD-L1 monotherapy(2).

208 olumab plus ipilimumab for anti-PD-1 or anti-PD-L1-naive disease, and durvalumab plus tremelimumab fo

209 d that interference with platelet binding to PD-L1 negative cancer cells promotes T cell-induced canc

210 atelet-derived PD-L1 regulates the growth of PD-L1 negative tumors and that interference with platele

211 es of PD-L1 based therapies in patients with PD-L1 negative tumors may be explained, in part, by the

212 Precisely why patients with PD-L1 negative tumors respond to PD-1/PD-L1 checkpoint i

213 higher in PD-L1-positive (8/28; 29%) versus PD-L1-negative (0/12; 0%) patients.

214 LRR-, and pyrin domain-containing protein 3 (PD-L1/NLRP3) inflammasome signaling cascade that ultimat

215 ed biomarker programmed cell death ligand 1 (PD-L1) nor tumor mutational burden differentiated PFS in

216 eveal an acetylation-dependent regulation of PD-L1 nuclear localization that governs immune-response

217 In this study, we explore the functions of PD-L1 on dendritic cells (DCs), which highly express PD-

218 and down-regulation of checkpoint regulator PD-L1 on the cancer cells.

219 hibitor that systemically binds and inhibits PD-L1 on tumor cells and immune cells.

220 ent in regulating programmed death-ligand 1 (PD-L1) on KSHV-carrying tumor cells.

221 une surveillance; this can be overcome using PD-L1 or PD-1 immunotherapy antibodies.

222 ses were observed regardless of tumor MCPyV, PD-L1, or TMB status.

223 The PD-L1-overexpressing platelets (designated PD-L1 platele

224 In conclusion, although targeting the PD-1/PD-L1 pathway reinvigorates exhausted CD8(+) T cells, it

225 cases of primary OASC were immunostained for PD-L1, PD-L2 and CD8.

226 ificantly higher levels of the PRMT1 targets PD-L1, PD-L2, and VISTA than those with the CC genotype.

227 quantify immunotherapy target proteins PD-1, PD-L1, PD-L2, IDO1, LAG3, TIM3, ICOSLG, VISTA, GITR, and

228 estrained effector T cells via the canonical PD-L1-PD-1 axis and were sufficient to accelerate tumori

229 Immunotherapy directed at the PD-L1/PD-1 axis has produced treatment advances in vario

230 can be used to quantify tumor uptake of the PD-L1 PET tracer (18)F-BMS-986192.

231 Moreover, PD-L1 platelet treatment also increases the percentage o

232 e PD-L1-overexpressing platelets (designated PD-L1 platelets) accumulate in the inflamed pancreas and

233 atients with high PD-L1 expression (the high PD-L1 population) and between the durvalumab plus tremel

234 In the high PD-L1 population, median overall survival was 14.4 month

235 erformed for real-time in vivo monitoring of PD-L1 positive tumor cells and CTLs with cellular resolu

236 Patients with PD-L1 positive tumours (>=1%) had significantly shorter

237 valuable), and response rates were higher in PD-L1-positive (8/28; 29%) versus PD-L1-negative (0/12;

238 In the PD-L1-positive population, pathological complete respons

239 able, with a 1-year survival of 52.1% in the PD-L1-positive population.

240 ; HR, 0.56; 95% CI, 0.47 to 0.68) and in the PD-L1-positive tumor subgroup (HR, 0.57; 99% CI, 0.43 to

241 ients with rare RCC, particularly those with PD-L1-positive tumors.

242 d responses were observed in only a few rare PD-L1-positive tumour types, suggesting that PD-L1 expre

243 arranted in a subpopulation of patients with PD-L1-positive, HER2-positive advanced breast cancer.

244 ents with melanoma or a centrally confirmed, PD-L1-positive, relapsed or refractory solid tumour or l

245 PD-L1 positivity appears to be predictive of pembrolizum

246 ate and multivariate analyses confirmed that PD-L1 protein expression is an independent prognostic ma

247 ession to promote apoptosis while decreasing PD-L1 protein levels to enhance the cytotoxic activity o

248 n factor O3a (FOXO3a) function and stabilize PD-L1 protein, respectively.

249 Here, we show that platelet-derived PD-L1 regulates the growth of PD-L1 negative tumors and

250 umab plus tremelimumab for anti-PD-1 or anti-PD-L1 relapsed disease.

251 mechanisms by which blocking IL-6, CD47 and PD-L1 reversed fibrosis, by increasing phagocytosis of p

252 d the FSY react with a proximal histidine of PD-L1 selectively, enabling irreversible binding of PD-1

253 PD-L1 signaling also induced an anergic T-bet(-)IFN-gamm

254 Inhibiting VISTA- and PD-L1-signaling relieved immune suppression and reduced

255 red KIF5B-RET fusion and had highly positive PD-L1 staining, received nivolumab as second-line treatm

256 antly shorter OS than patients with negative PD-L1 status (p = 0.031).

257 of triple-negative breast cancer status and PD-L1 status by immunohistochemistry at a central labora

258 fied according to disease stage and baseline PD-L1 status of tumour cells.

259 PD-L1 status was available for 36 patients; 15 (42%) had

260 ith stratification by cisplatin eligibility, PD-L1 status, and presence or absence of liver metastase

261 s are conditional on the basis of histology, PD-L1 status, and/or the presence or absence of contrain

262 as determined by programmed death-ligand 1 (PD-L1) status, and on-therapy quality-of-life (QOL) metr

263 Here we show that PD-L1 switches TNFalpha-induced apoptosis to pyroptosis

264 CR4 in combination with blockade of the PD-1/PD-L1 T cell checkpoint induces T cell infiltration and

265 even in the absence of endogenous PD-L1; (3) PD-L1(+) T cells engaged PD-1(+) macrophages, inducing a

266 Collectively, we demonstrate that PD-L1(+) T cells have diverse tolerogenic effects on tum

267 suppressive compared to PD-1 signaling; (2) PD-L1(+) T cells restrained effector T cells via the can

268 In a murine model of CCA, recruited PD-L1+ TAMs facilitated CCA progression.

269 er negative (0%) or low positive (1% to 49%) PD-L1, the Expert Panel recommends pembrolizumab/carbopl

270 315 patients responded to anti-PD-1 or anti-PD-L1 therapy for immunotherapy-naive disease, and three

271 onclusion, combined MAPK inhibition and anti-PD-L1 therapy may provide treatment options for patients

272 cells, overcomes acquired resistance to anti-PD-L1 therapy, and establishes tumor-specific immunologi

273 otherapy combinations for anti-PD-1 and anti-PD-L1 therapy-relapsed disease.

274 umors, and renders tumors responsive to anti-PD-L1 therapy.

275 xic T lymphocytes (CTLs) in response to anti-PD-L1 therapy.

276 ificant mechanism of resistance to anti-PD-1/PD-L1 therapy.

277 hotopic tumor mouse models resistant to anti-PD-L1-therapy, we are testing the hypothesis that in sit

278 Tumor cells secrete PD-L1 through exosomes or splice variants, which has bee

279 ls are genetically engineered to overexpress PD-L1 to produce immunosuppressive platelets.

280 sponses did not correlate with expression of PD-L1, total mutation burden, or an interferon-gamma gen

281 1 CPS >=1 was detected in 95% of OASC, while PD-L1 TPS >=1 was found in 75%.

282 -based human programmed cell death ligand 1 (PD-L1) tracer, was developed to noninvasively determine

283 e expression, and thereby advocate targeting PD-L1 translocation to enhance the efficacy of PD-1/PD-L

284 Nevertheless, anti-PD-L1-treated mice showed an even more narrowed TCR repe

285 Using anti-PD-1 or anti-PD-L1 treatment against earlier stages of cancer is hypo

286 Anti-PD-L1 treatment restricts tumor growth in mice bearing A

287 sensitized melanoma cells to anti-PD-1/anti-PD-L1 treatment.

288 In vivo, IFNgamma affected neither PD-L1 tumor expression measured immunohistochemically no

289 as a critical therapeutic target to suppress PD-L1 tumor-intrinsic function.

290 ed CD8 + T-cells and PD-L1 + macrophages and PD-L1 + tumor cells as mechanistic determinants of respo

291 a reduction in type 1 regulatory T cells and PD-L1+ tumor-associated macrophages at this early time p

292 We retrospectively studied PD-L1 tumour proportion score and Ki-67 index in pleural

293 cally advanced or metastatic, HER2-positive, PD-L1-unselected gastro-oesophageal adenocarcinoma, with

294 ntial for PD-L1 blockade and they upregulate PD-L1 upon antigen uptake.

295 This phenotype maps to defective PD-L1 upregulation on mutant tumor cells, which improves

296 enting tumor antigens to T cells, subsequent PD-L1 upregulation protects them from killing by cytotox

297 henotypes, including enhanced cell invasion, PD-L1 upregulation, and chemoresistance, were sustained

298 Administration of rhIL-15/anti-PD-L1 was safe and well tolerated.

299 histochemistry (IHC) and MS measurements for PD-L1 were weakly correlated, but IHC did not distinguis

300 Atezolizumab is an inhibitor of PD-L1, which can lead to enhanced anticancer T-cell acti