ライフサイエンスコーパス: PD

1 PD arterioles exhibited particular upregulation of the c

2 PD-1 identifies "exhausted" CD8 T cells with impaired HI

3 PD-1 inhibitory receptor blockade partially reversed T c

4 PD-1 is expressed by CD56(dim) but not CD56(bright) NK c

5 PD-1 was recently shown to be expressed on and thereby i

6 PD-L1 positivity was defined as expression by immunohist

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

8 hanism for regulation of programmed death 1 (PD-1) and its ligand (PD-L1) is partially understood.

9 checkpoint blockade with programmed death 1 (PD-1) targeted agents, novel immunotherapies and combina

10 that inhibits PD-L1 and programmed death-1 (PD-1) and PD-L1 and B7-1 interactions, reinvigorating an

11 1 (PD-L1) interacts with programmed death-1 (PD-1) and the immunostimulatory molecule CD80 and functi

12 Programmed cell death-1 (PD-1)-targeted therapies enhance T cell responses and sh

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

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

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

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

17 ing between programmed cell death protein 1 (PD-1) and the PD-1 ligands (PD-L1, PD-L2) is essential f

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

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

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

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

22 PPA and PPRF arms were 8 and 6 DOT per 1000 PD, respectively (P = .03).

23 and Methods For this retrospective study, 15 PD + VH patients, 40 PD - VH patients, and 15 control pa

24 trate that programmed cell death 1 ligand 2 (PD-L2) regulates the production of natural Abs against p

25 r expression patterns of 2B4, CTLA-4, LAG-3, PD-1, and Tim-3 on virus-specific CD4 and CD8 T cells in

26 Of 305 PD survivors, 245 (80.3%) responded, of whom 157 (64.1%)

27 retrospective study, 15 PD + VH patients, 40 PD - VH patients, and 15 control participants from a pro

28 A training dataset of 51 PD patients with STN DBS was combined with publicly avai

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

30 e progression had either a delayed or absent PD-1+ CD8 T-cell response, whereas 80% of patients with

31 d 1 (PD-L1)-mediated inhibition of activated PD-1(+) T lymphocytes plays a major role in tumor escape

32 In addition, PD, PI, BOP, MR, and SUP varied significantly according

33 nt with a blocking antibody directed against PD-1.

34 ing an institutional database containing all PDs performed 2002 to 2012 at a single institution, incl

35 .4 [12.2] years) detected increased PD-1 and PD-L2 expression in high-risk cSCC.

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

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

38 not show significant differences in CAL and PD compared with untreated patients with hypertriglyceri

39 ination treatment with CDK4/6 inhibitors and PD-1-PD-L1 immune checkpoint blockade to enhance therape

40 However, the role of PD-L1 and PD-1 in regulating pain and neuronal function is unclear

41 Expression of PD-1 and its ligands PD-L1 and PD-L2 in chronic rhinosinusitis with nasal polyps (CRSwN

42 lated that of HLA class I, B7-H3, PD-L1, and PD-L2, molecules that might limit NK cell function.

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

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

45 ide unique insight into specific uremia- and PD-induced pathomechanisms of CVD.

46 edefining the continuum between seizures and PDs, suggesting that additional damage after acute brain

47 bination of the PC7A nanovaccine and an anti-PD-1 antibody showed great synergy, with 100% survival o

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

49 owever, even when using anti-CTLA-4 and anti-PD-1 in combination, approximately half of patients exhi

50 Moreover, addition of an antagonistic anti-PD-1 antibody increased cell death in 3D spheroids and e

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

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

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

54 how tumor and immunity co-evolve during anti-PD-1 therapy.

55 ctive antitumor immune responses during anti-PD-1 treatment in mice.

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

57 nt of phenformin enhances the effect of anti-PD-1 antibody therapy on inhibiting tumor growth in the

58 significantly increased the efficacy of anti-PD-1 checkpoint blockade.

59 ompt recognition and discontinuation of anti-PD-1 therapy is recommended.

60 pattern also observed in other cases of anti-PD-1-induced lichenoid dermatitis.

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

62 bination therapy of ISF35 with systemic anti-PD-1 generates greater antitumor activity than each resp

63 ar serous retinal detachment related to anti-PD-1 treatment, and the first with nivolumab.

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

65 than Vss subfamilies not amplified upon anti-PD-1 therapy and could be identified by a sustained coex

66 ngal infection and to determine whether anti-PD-1 Ab treatment improves fungal clearance.

67 stion of improved benefit compared with anti-PD-1 monotherapy in patients with NSCLC, supporting furt

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

69 ion in cancer therapy to a similar degree as PD-1 blocking antibodies, offering a next-generation app

70 ion in cancer therapy to a similar degree as PD-1-blocking antibodies.Significance: These findings sh

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

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

73 GD, mediates PD pathology in GBA-associated PD.

74 ions of chromosome 9p24.1 and the associated PD-1 ligand loci, CD274/PD-L1 and PDCD1LG2/PD-L2, and co

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

76 nnectivity pattern in the cerebellum between PD patients and healthy controls.

77 Furthermore, blocking PD-1 with an antibody increased KLRG1(+) ILC-2 cell numb

78 First, both PD patients and mice with ventral tegmental area (VTA) d

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

80 1 and the associated PD-1 ligand loci, CD274/PD-L1 and PDCD1LG2/PD-L2, and copy number-dependent incr

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

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

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

84 Additionally, we compared PD values of groups with longer and shorter distances th

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

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

87 We demonstrate that the frequency of CXCR5(+)PD-1(+)ICOS(+)-activated circulating Tfh cells is increa

88 Naive PD-L2-deficient (PD-L2(-/-)) mice produced significantly more PC-reactive

89 lative to the median angle (-8.13 degrees ), PD values decreased in lower nasal (ADSP: -0.11 dB) and

90 ex (mSBI), plaque index (PI), probing depth (PD), and clinical attachment level (CAL).

91 leeding on probing [BOP], and probing depth [PD] >/=4 mm) and crestal bone loss (CBL) around immediat

92 Pattern deviation (PD) values of 11,449 reliable visual fields (VFs) that a

93 Peritoneal dialysis (PD) is a life-saving form of renal replacement therapy f

94 ltration in patients on peritoneal dialysis (PD).

95 e-wide association study with a dimensional, PD/AG-related anxiety phenotype based on the Agoraphobia

96 the medical management of Parkinson disease (PD) during Ramadan.

97 duced dyskinesia (LID) in Parkinson disease (PD) is an unmet need.

98 ment (MCI), patients with Parkinson disease (PD), and young and older healthy volunteers.

99 ggest a greater risk of Parkinson's disease (PD) after traumatic brain injury (TBI), but it is possib

100 The motor symptoms of Parkinson's disease (PD) are linked to abnormally correlated and coherent act

101 ile the pathogenesis of Parkinson's disease (PD) is incompletely understood, mitochondrial dysfunctio

102 A major hallmark of Parkinson's disease (PD) is the presence of Lewy bodies (LBs) in certain neur

103 has a prominent role in Parkinson's disease (PD) pathology.

104 Parkinson's disease (PD) patients experience loss of normal motor function (h

105 bility of patients with Parkinson's disease (PD) to maximize monetary rewards and minimize physical e

106 n stimulation (DBS) for Parkinson's disease (PD) under local or general anaesthesia exist, and there

107 ative disorders such as Parkinson's disease (PD), it is important to examine how AgNPs affect microgl

108 thologic contributor to Parkinson's disease (PD).

109 sed risk for developing Parkinson's disease (PD).

110 ation is a key event in Parkinson's disease (PD).

111 hology in patients with Parkinson's disease (PD).

112 et for the treatment of Parkinson's disease (PD).

113 dopaminergic neurons in Parkinson's disease (PD).

114 ial prodromal marker of Parkinson's disease (PD).

115 omplex diseases such as Parkinson's Disease (PD).

116 for the development of Parkinson's disease (PD).

117 f familial and sporadic Parkinson's disease (PD).

118 alpha-synuclein lead to Parkinson's disease (PD).

119 on of neuropathology in Parkinson's disease (PD).

120 common cause of genetic Parkinson's disease (PD).

121 The molecular genetics of panic disorder (PD) with and without agoraphobia (AG) are still largely

122 ized anxiety disorder (GAD), panic disorder (PD), and phobias (agoraphobia, social phobia, etc.).

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

124 show how GSK-3 inhibitors that downregulate PD-1 expression can enhance CD8(+) T-cell function in ca

125 show how GSK-3 inhibitors that downregulate PD-1 expression can enhance CD8(+) T-cell function in ca

126 loration of other strategies to downregulate PD-1 for cancer therapy.

127 at blockade of STAT3 signaling downregulated PD-1/PD-L1 in a Tgfbr1/Pten 2cKO HNSCC mouse model.

128 In early PD, EDS increases significantly over time and is associa

129 sting in a phase III clinical trial in early PD.

130 of patients with clinical benefit exhibited PD-1+ CD8 T-cell responses within 4 wk of treatment init

131 ell established that viral pathogens exploit PD to spread between cells, but it has more recently bee

132 or-infiltrating lymphocytes (TIL) expressing PD-1 can recognize autologous tumor cells, suggesting th

133 scattered CD20+ B cells, and relatively few PD-1+ (programmed cell death 1-positive) T cells, an imm

134 elated inpatient costs for 90 days following PD, converted to 2014 $USD.

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

136 ding glucocerebrosidase are risk factors for PD, indicating that disrupted GSL clearance plays a key

137 drain placement and early drain removal for PD.

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

139 Mean values for PD and CAL in the two hypertriglyceridemic groups were s

140 or cells, suggesting that cells derived from PD-1(+) TILs can be used in adoptive T-cell therapy (ACT

141 In vivo, only cells expanded from PD-1(+) CD8 TILs contained tumor progression, and their

142 gated in distinct leukocyte populations from PD patients with depression and those without depression

143 ADC maps (98%, 95 of 97 patients) than on FS PD-weighted TSE images (86%, 84 of 97 patients) (P < .00

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

145 mean [SD] age, 55 [15] years), 32 (36%) had PDs on sEEG and dEEG recordings and 21 (23%) on dEEG rec

146 In contrast, activated ICOS(hi) PD-1(hi) circulating T follicular helper (Tfh) cells dec

147 The structure of TcPINK1 explains how PD-linked mutations that lie within the kinase domain re

148 rkinKO mice, however, poorly represent human PD symptoms as they only exhibit mild motor phenotypes,

149 acy and safety of pembrolizumab, a humanized PD-1-blocking antibody, at a dose of 200 mg every 3 week

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

151 iron from various brain regions and improve PD symptomology.

152 baseline 5.6 (4.1) to 7.7 (5.0) at year 2 in PD subjects (p<0.001) versus from 2.9 (3.0) to 3.2 (3.0)

153 that submucous neurons were not affected in PD patients, which suggests that these neurons are not i

154 antification of noradrenergic denervation in PD patients in vivo.

155 Longitudinally, EDS in PD was associated with non-tremor dominant phenotype, au

156 itating each other's pathogenic functions in PD.

157 Risk of TBI was greater in PD patients in their prodromal period across all age and

158 n integrated HIV DNA per 10-unit increase in PD-1+ CD4+ T cells; 95% CI = 1.01-2.05; P = .045) and CD

159 iferation of GABAergic pallido-STN inputs in PD mice, reduced loss of cortico-STN transmission and pa

160 can be used for therapeutic intervention in PD.

161 of novel loci and their pathways involved in PD and autoimmune diseases.

162 neurons while exhibiting milder cell loss in PD, we aimed to define the electrophysiological properti

163 tial progression pattern of dopamine loss in PD.

164 ur in absence of dopaminergic neuron loss in PD.

165 novel strategies for disease modification in PD and other synucleinopathies.

166 s effective in improving muscle pathology in PD mice injected intramuscularly with an AAV-TFEB vector

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

168 s a disease-modifying treatment principle in PD.

169 k for planning disease prevention studies in PD.

170 sociated with multiple non-motor symptoms in PD and have important clinical consequences, including t

171 significantly lower in MSA-P and PSP than in PD and MSA-C patients and might therefore be of interest

172 We identified 89,790 incident PD cases and 118,095 comparable controls aged > 65 years

173 f ADCs with immuno-oncology drugs, including PD-1 or PD-L1 antibodies, OX40 ligand, or GITR ligand fu

174 ] age, 76.4 [12.2] years) detected increased PD-1 and PD-L2 expression in high-risk cSCC.

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

176 ants of alphaS are correlated with inherited PD.

177 1 (PD-L1) monoclonal antibody that inhibits PD-L1 and programmed death-1 (PD-1) and PD-L1 and B7-1 i

178 were missing data for either race or initial PD modality.

179 Thus, B-1 cell-intrinsic PD-L2 expression inhibits IL-5 production by T cells and

180 ical analysis for immune checkpoints (PD-L1, PD-1, LAG-3) and immune cell (IC) subsets (CD3, CD4, CD8

181 rotein 1 (PD-1) and the PD-1 ligands (PD-L1, PD-L2) is essential for malignant Hodgkin Reed-Sternberg

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

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

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

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

186 Using purified components, and Loqs-PD truncations, we provide a mechanistic basis for Loqs-

187 ons, we provide a mechanistic basis for Loqs-PD functions.

188 by downregulation of the exhaustion markers PD-1 and LAG-3.

189 were observed between JP2 presence and mean PD (P <0.002) and CAL (P <0.001), after therapy.

190 ed significant reductions (P < 0.05) of mean PD (1.4 +/- 0.7 mm), clinical attachment level (CAL) (1.

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

192 a sphingolipid accumulating in GD, mediates PD pathology in GBA-associated PD.

193 al inclusion bodies at structurally modified PDs in cells coexpressing 6K2, CI, and P3N-PIPO.

194 ed high levels of the coinhibitory molecules PD-1, Lag-3, and TIGIT, thereby limiting NK cell-mediate

195 stural instability and gait difficulty motor PD subtype in linear regression analysis, but staging of

196 Naive PD-L2-deficient (PD-L2(-/-)) mice produced significantly

197 haSyn-induced cell death in a human neuronal PD model.

198 In the absence of PD-ligands, both TS1 TEM and TN induced late-onset myoca

199 severe skin and liver GVHD in the absence of PD-ligands.

200 l cytotoxicity when neutralizing antibody of PD-1 or PD-L1 was added.

201 oradrenergic projections in vivo in brain of PD patients.

202 uently appears to propagate in the brains of PD patients following a stereotypic pattern consistent w

203 esent the most common known genetic cause of PD.

204 g in the neurodegeneration characteristic of PD.SIGNIFICANCE STATEMENT Disruptions or alterations in

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

206 be identified by a sustained coexpression of PD-1 and TIGIT receptors.

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

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

209 have a causative role in the development of PD are expressed in astrocytes and have important roles

210 stmortem analyses confirmed the diagnosis of PD and demonstrated >300,000 tyrosine hydroxylase (TH)-p

211 Strikingly, signaling downstream of PD-1 in purified T cell subsets did not correlate with P

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

213 ed mice ameliorated the antitumor effects of PD-1 blockade, whereas FMT from nonresponding patients f

214 1 expression and heterogeneity evaluation of PD-L1 expression across tumors in the same subject.

215 Expression of PD-1 and its ligands PD-L1 and PD-L2 in chronic rhinosin

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

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

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

219 6192 bound to tumor tissues as a function of PD-L1 expression determined by immunohistochemistry.

220 The impact of PD-1 immune checkpoint therapy prompts exploration of ot

221 and PTL and support further investigation of PD-1 blockade in these diseases.

222 Using a rat model of PD, partial elimination of the functional interaction be

223 chemogenetic stimulation in rodent models of PD (PD mice) and L-DOPA-induced dyskinesia (LID mice).

224 europrotective in mouse neurotoxin models of PD, and isradipine is currently undergoing testing in a

225 eceptor (S1PR) agonist, on 2 mouse models of PD.

226 non-FRC users (mean difference in number of PD sites: 6.9, 5.6, and 5.6; P <0.05; mean difference in

227 of TBI is greater in the prodromal period of PD.

228 h revealed a markedly expanded population of PD-1(hi)CXCR5(-)CD4(+) T cells in synovium of patients w

229 Additionally, the presence of PD-related human alpha-synuclein A53T mutant or dopamine

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

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

232 gher BMI was associated with a lower risk of PD (OR 0.82, 95% CI 0.69-0.98).

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

234 ogenesis or the gastrointestinal symptoms of PD.

235 f the pathogenic process and therapeutics of PD.

236 a strong association between variability of PD-1 and Tim-3 expression by T cells and infectious epis

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

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

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

240 d A53T alpha-synuclein (aSyn)-overexpressing PD rat model (AAV1/2-A53T-aSyn).

241 outcomes following pancreaticoduodenectomy (PD) for patients treated at local, low-volume centers an

242 plication following pancreaticoduodenectomy (PD), associated with significant morbidity and healthcar

243 nagement protocol for pancreatoduodenectomy (PD).

244 of CP (P = 0.008) and periodontal parameters PD, CAL, and BOP was identified.

245 ogenetic stimulation in rodent models of PD (PD mice) and L-DOPA-induced dyskinesia (LID mice).

246 Pdcd1 (PD-1) disruption augmented CAR T cell mediated killing o

247 d PD-1 ligand loci, CD274/PD-L1 and PDCD1LG2/PD-L2, and copy number-dependent increased expression of

248 chronic inflammatory disease periodontitis (PD).

249 ontrol sample with the categorical phenotype PD/AG (Ncombined =1012) obtaining highly significant P-v

250 This PK-PD model mimics the human condition and can be applied t

251 Potential PK/PD predictors included 0- to 24-hour area under the curv

252 king of proteins required for plasmodesmata (PD) development, as well as the transport of some ion tr

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

254 We investigated p11 levels in postmortem PD brains and assessed whether peripheral p11 levels cor

255 for performance enhancement of self-powered PDs.

256 The PREDICT-PD algorithm identifies a population with an increased r

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

258 aiding vascular communication among the PT, PD, and brain.

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

260 Mechanistically, IRF4 repressed PD-1, Helios, and other molecules associated with T cell

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

262 The PD patient exomes were compared to 884 control exomes se

263 ogrammed cell death protein 1 (PD-1) and the PD-1 ligands (PD-L1, PD-L2) is essential for malignant H

264 perturbations of fibril conformation by the PD-related mutations that are not apparent through trans

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

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

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

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

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

270 al under such conditions is dependent on the PD-1/PD-L1 coinhibitory pathway.

271 tion and at a -0.45% compressive strain, the PD's photocurrent is dramatically enhanced from approxim

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

273 Rs consistently increasing with proximity to PD diagnosis.

274 In this near-complete response to PD-1 blockade in a mesenchymal tumor, we identified PTEN

275 features are associated with the response to PD-1 blockade in other tumour types.

276 CI is directed to PDs through its interaction with P3N-PIPO.

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

278 might be therapeutically bolstered to treat PD.

279 s to centralize care for patients undergoing PD.

280 f SNCA is of utmost importance to understand PD pathology.

281 3%) responded, of whom 157 (64.1%) underwent PD for nonmalignant lesions.

282 pathogens can spread between host cells via PD.

283 tween cells, raising questions about whether PD are in different functional states during different i

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

285 rified T cell subsets did not correlate with PD-1 surface expression but was inversely correlated wit

286 associations between integrated HIV DNA with PD-1+ CD4+ T-cells (1.44 fold-change in integrated HIV D

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

288 treatment of ovarian tumor-bearing mice with PD-1 blocking antibody resulted in an increase in IL10 l

289 Mean number of sites per participant with PD >/=4, >/=6, and >/=8 mm and AL >/=3, >/=5, and >/=8 m

290 We studied a cohort of 43 patients with PD (12 with an ICD and 31 without) undergoing DBS electr

291 Results Three patients with PD and four subjects with MCI were excluded because of e

292 Results Patients with PD and MCI had global network alterations when compared

293 y off-time in levodopa-treated patients with PD and motor fluctuations, and this effect is maintained

294 Of note, patients with PD observed during RBD episodes exhibit improved motor f

295 ed single unit activity in ten patients with PD who performed repetitive feet or hand movements while

296 with both control subjects and patients with PD without MCI (range, P = .004 to P = .048).

297 and nonmotor complications in patients with PD, and we performed a meta-analysis to identify the pat

298 and thus cognitive deficits in patients with PD.

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

300 ycerol kinase zeta (DGKzeta) with or without PD-1/PD-L1 blockade.