ライフサイエンスコーパス: exhaustion

1 e, chronic immune activation leads to T-cell exhaustion.

2 closely resembled self-tolerance than viral exhaustion.

3 -chain-dependent cytokines, on CD8(+) T-cell exhaustion.

4 eed, poor appetite, physical inactivity, and exhaustion.

5 -1, Lag-3, and TIGIT, indicative of cellular exhaustion.

6 ance to 5-FU-induced hematopoietic stem cell exhaustion.

7 3), thereby facilitating intratumoral T cell exhaustion.

8 eventual programmed death 1-mediated T cell exhaustion.

9 led to increased proliferation and stem-cell exhaustion.

10 f CD56, a phenotype associated with NK cells exhaustion.

11 ice, a phenotype that is associated with HSC exhaustion.

12 unction despite expressing markers of severe exhaustion.

13 ursor frequencies due to irreversible T cell exhaustion.

14 horiomeningitis clone 13 and reversed T cell exhaustion.

15 pressed markers implicating a role in T-cell exhaustion.

16 sma interleukin-8 associated with neutrophil exhaustion.

17 ation of multiple pathways implicated in HSC exhaustion.

18 r persistent infections with signs of T cell exhaustion.

19 hickness, accompanied by epidermal stem cell exhaustion.

20 onically activated Th1 cells from undergoing exhaustion.

21 pansion and tumor eradication while reducing exhaustion.

22 hus suggesting immunosuppression rather than exhaustion.

23 isease and show progressive accumulation and exhaustion.

24 e of the cell-intrinsic mechanisms of T cell exhaustion.

25 d by an elevated CD8/CD4 ratio and decreased exhaustion.

26 n factor NFAT controls the program of T cell exhaustion.

27 on melanoma cells and associated with T-cell exhaustion.

28 erall pattern that bears hallmarks of T cell exhaustion.

29 nses during Plasmodium-induced CD4(+) T cell exhaustion.

30 unclear whether PD-1 directly causes T cell exhaustion.

31 a gene expression program involved in T cell exhaustion.

32 onic infection and exacerbated CD8(+) T cell exhaustion.

33 wo of the major causes of muscle fatigue and exhaustion.

34 ytomegalovirus with only limited evidence of exhaustion.

35 ates ranging from effector memory T cells to exhaustion.

36 e features of both activation and functional exhaustion.

37 delaying effector T-cell differentiation and exhaustion.

38 atigue, cognitive dysfunction and exertional exhaustion.

39 racterized by NK cell dysfunction and T cell exhaustion.

40 TCR) and CAR be engaged to accelerate T cell exhaustion.

41 memory compartment and contribute to B cell exhaustion.

42 74.7% had heat exhaustion, 5.4% heat stroke.

43 Chronic infections result in T-cell exhaustion, a state of functional unresponsiveness.

44 to four different running intensities until exhaustion, accomplished in a non-motorized treadmill us

45 mmed death-1-mediated (PD-1-mediated) T cell exhaustion affects mesothelin-targeted CAR T cells and e

46 itory receptors and exhibited transcriptomic exhaustion and anergy profiles by gene set enrichment an

47 VHD-targeted tissues resulted in CD8+ T cell exhaustion and apoptosis, thereby preventing GVHD, where

48 ylation programming as a regulator of T cell exhaustion and barrier of ICB-mediated T cell rejuvenati

49 stress to critical care nurses and emotional exhaustion and burnout can arise from such dissonance be

50 iptional mechanisms regulating CD8(+) T cell exhaustion and cell death are poorly defined.

51 ell response that is characterized by T cell exhaustion and cell death of Ag-specific CD8(+) T cells.

52 of effector T cells, promoted expression of exhaustion and coinhibitory markers on T cells, and syne

53 nipulating the host response to increase the exhaustion and depletion of protective CD4 T cells.

54 es of CD4(+) versus CD8(+) T-cell senescence/exhaustion and effects of antiretroviral therapy (ART) o

55 evelop a molecular signature consistent with exhaustion and failure to participate in antimicrobial d

56 ngs provide a better understanding of T-cell exhaustion and have implications in the optimization of

57 ia (CLL), CD8(+) T cells exhibit features of exhaustion and impaired functionality.

58 (PD-L1) interaction with PD-1 induces T cell exhaustion and is a therapeutic target to enhance immune

59 mammary epithelial stem cell quiescence and exhaustion and is necessary for long-term maintenance of

60 hronic SIV infection, despite high levels of exhaustion and likely inhibition by Foxp3(+) cells, a su

61 MAPKi therapy preceded CD8 T cell deficiency/exhaustion and loss of antigen presentation in half of d

62 tochondrial dysfunction, satellite cell (SC) exhaustion and loss of skeletal and cardiac muscle funct

63 -related human hematopoietic stem cell (HSC) exhaustion and myeloid-lineage skewing promote oncogenic

64 LRG1, all receptors associated with cellular exhaustion and NK cell memory.

65 Functional exhaustion and numerical reduction of HBV-specific cytot

66 ir sustained hyperexpression promotes immune exhaustion and paralysis.

67 r to mouse islets, human islets exhibit cell exhaustion and recovery in response to transient hypergl

68 data demonstrate a major role of functional exhaustion and recovery of beta-cells during T1D onset a

69 une serum prevented CD8(+) T cell functional exhaustion and reduced mortality in mice lacking B cells

70 wild-type HSPCs are absent, leading to their exhaustion and reduced survival of recipients.

71 portion of naive T cells, evidence of T cell exhaustion and senescence, and variable loss of T cell C

72 KT recipients with exhaustion and slowed walking speed (hazards ratio = 2.4

73 light a key metabolic control event early in exhaustion and suggest that manipulating glycolytic and

74 activation ultimately leads to severe T cell exhaustion and the inability of the host to control vira

75 omeres have been associated with replicative exhaustion and tissue failure.

76 bles was associated with a decreased risk of exhaustion and unintentional weight loss.

77 e rapidly replicating LCMV-WE induced T cell exhaustion and viral persistence.

78 ough inhibitory receptors often cause T cell exhaustion and viral spreading during chronic viral infe

79 levels of PD-1, TIM-3, and CTLA-4 markers of exhaustion, and (iii) produced less tumor necrosis facto

80 mune response, but terminal differentiation, exhaustion, and apoptosis in the activated effector T ce

81 ith PD-1 on donor CD8+ T cells cause anergy, exhaustion, and apoptosis, thereby preventing GVHD.

82 uded features of endotoxin tolerance, T-cell exhaustion, and downregulation of human leucocyte antige

83 r inducing systemic inflammation, neutrophil exhaustion, and exacerbating hepatic encephalopathy.

84 ion is associated with B cell activation and exhaustion, and hypergammaglobulinemia.

85 e, grip strength, self-reported weight loss, exhaustion, and low activity.

86 ith Instrumental Activities of Daily Living, exhaustion, and low physical activity (P < 0.001 for eac

87 ly, as well as markers of T-cell activation, exhaustion, and maturation.

88 the mechanisms involved in reversing T cell exhaustion, and outline critical areas of focus for futu

89 s anti-CTLA4, demonstrated persistent T-cell exhaustion, and rapidly progressed.

90 etry to detect markers of T cell maturation, exhaustion, and senescence known to influence immune fun

91 loss, low physical activity level, weakness, exhaustion, and slow gait speed), and incident CVD as on

92 ; 95% CI, 1.17-5.03) and poor grip strength, exhaustion, and slowed walking speed (hazard ratio, 2.61

93 activation can be a driving force in immune exhaustion, and type I interferons (IFN-I) are emerging

94 haracterized by the combination of weakness, exhaustion, and weight loss.

95 PD-1-targeted therapies reverse TCD8 exhaustion/anergy.

96 ne activation, immunosuppression, and T cell exhaustion are hallmarks of HIV infection, yet the mecha

97 In fact, some aspects of exhaustion are more severe with genetic deletion of PD-1

98 nd telomere loss with subsequent replicative exhaustion as a mechanism for refractory gut GVHD that i

99 D-1 therapy demonstrated a release of T cell exhaustion, as measured by an accumulation of highly act

100 Here, we show that a soluble form of T cell exhaustion associated coinhibitory molecule 3, sTim-3, i

101 Moreover, these exhaustion-associated DNA-methylation programs were acqu

102 timulation is reduced by signals through the exhaustion-associated inhibitory receptor PD-1, suggesti

103 ecular dynamics simulations of one potential exhaustion-associated system: the complex of human inhib

104 course and potentially experience beta-cell exhaustion at a younger age.

105 itochondrial oxidative capacity, run time to exhaustion at various intensities was impaired in the KO

106 ta show that NFAT promotes T cell anergy and exhaustion by binding at sites that do not require coope

107 Satb1 functions to prevent premature T cell exhaustion by regulating Pdcd1 expression upon T cell ac

108 atechin) progressively prolonged the time to exhaustion by threefold longer than the control, fruit o

109 These results demonstrate that CD8(+) T cell exhaustion can occur in the absence of PD-1.

110 tate to avoid genomic insults and to prevent exhaustion caused by excessive proliferation.

111 reas markers of CD4(+) T-cell senescence and exhaustion (CD4(+)CD28(-)CD57(+)PD1(+)) and CD4(+) T-cel

112 rapeutic target for reversing the neurogenic exhaustion characteristic of the aged OE.

113 chromatin accessibility specific for T-cell exhaustion, characterized by enrichment for consensus bi

114 bjects, chronic immune activation and T cell exhaustion contribute to the eventual deterioration of t

115 This exhaustion could contribute to the robust replication of

116 tool comprised of three subscales-emotional exhaustion, depersonalization, and achievement.

117 available regarding the extent of lymphocyte exhaustion development in the transplant setting and its

118 eath 1 (PD-1) on CD8 T cells promotes T cell exhaustion during chronic Ag exposure.

119 ttention as a key regulator of CD8(+) T cell exhaustion during chronic infection and cancer because b

120 The development of CD8 T-cell exhaustion during chronic infection is driven both by pe

121 he roles of the PD-1:PD-L1 pathway in T cell exhaustion during chronic infection.

122 the connection between this state and T cell exhaustion during chronic infections are unknown.

123 T cell exhaustion during chronic viral infection is well descri

124 -2 and IL-15 as instigators of CD8(+) T-cell exhaustion during chronic viral infection.

125 egulatory B cell that may precipitate T cell exhaustion during VL.

126 activation, proliferation, and CD8(+) T-cell exhaustion, during the earliest months of infection.

127 cell infiltration, reduced markers of T-cell exhaustion, elevated levels of proteins associated with

128 ophagy, mitochondrial dysfunction, stem cell exhaustion, epigenetic changes, abnormal microRNA profil

129 imp-1 is a critical regulator for CD4 T cell exhaustion especially in the CD4 central memory cell sub

130 her expression of GAL genes prior to glucose exhaustion experience a larger upfront growth cost but a

131 he present study, we hypothesize that T-cell exhaustion following infection is induced by the upregul

132 Although CD8 exhaustion has been previously reported in Toxoplasma en

133 Although exhaustion has most commonly been studied in the context

134 D-L1) pathway, a central regulator of T cell exhaustion, have been recently shown to be effective for

135 ng CD4(+) T cells ) and CD4(+)/CD8(+) T-cell exhaustion (ie, the percentage of PD-1(+) cells among CD

136 tic mice displayed exacerbated CD8(+) T cell exhaustion illustrated by increased inhibitory molecule

137 sengagement from HCV, whereas virus-specific exhaustion imparts a durable inhibitory imprint on cell

138 Lag-3, CD160, and 2B4 as a measure of T-cell exhaustion in a cohort of elite controllers and in chron

139 ce for the molecular understanding of T-cell exhaustion in cancer and other inflammatory settings.

140 y miR-31 as an important regulator of T cell exhaustion in chronic infection.

141 gram exhibited features distinct from T cell exhaustion in chronic infections.

142 ugh STAT5 as a potential mechanism of T cell exhaustion in chronic T. cruzi infection.

143 lved in tolerance and shown to induce T-cell exhaustion in chronic viral infection and cancers.

144 gling the molecular mechanisms of anergy and exhaustion in human B cells.

145 at PD-1 is not required for the induction of exhaustion in mice with chronic lymphocytic choriomening

146 ional factor Foxo3a cooperate to prevent HSC exhaustion in mice.

147 blocking Ab to reverse tumor-induced T cell exhaustion in NSCLC patients.

148 e mechanistic insights into human CAR T cell exhaustion in solid tumors and suggest that PD-1/PD-L1 b

149 Mechanisms that govern PD1 expression and exhaustion in T cells are not fully understood.

150 hts the major challenge of overcoming T-cell exhaustion in the context of persistent antigen exposure

151 eutrophil activation or increased neutrophil exhaustion in the GRK5 KO mice.

152 V replication was likely caused by localized exhaustion in the liver, where CD8(+) T-cell expression

153 he levels of HSV-1 latency and, thus, T-cell exhaustion in the TG of ocularly infected mice.IMPORTANC

154 igeminal ganglia (TG), and markers of T cell exhaustion in the TG were determined.

155 ificant differences in markers of functional exhaustion, including increased expression of IFN-gamma

156 he TME expressed multiple markers for T-cell exhaustion, including PD-1, Lag-3, and Tim-3 compared wi

157 Our work defines a novel mechanism of immune exhaustion induced by CD20 mAb in human NK cells, with p

158 gments, whereas 4-1BB costimulation reduces, exhaustion induced by persistent CAR signaling.

159 ring chronic infection the process of T-cell exhaustion inhibits the immune response, facilitating vi

160 T-cell exhaustion is a progressive loss of effector function an

161 nscriptional signature reflecting CD8 T-cell exhaustion is associated with poor clearance of chronic

162 p16, telomere attrition, and accompanied CPC exhaustion is evident in NS+/- mice.

163 ts, the kinetics of its development, whether exhaustion is influenced positively or negatively by dif

164 timulation is pronounced, that of CD8 T-cell exhaustion is reduced.

165 e of lung TCD8 more closely resembles T cell exhaustion late into chronic infection than do functiona

166 as independently associated with having less exhaustion, less depersonalization, a greater sense of p

167 g gammadeltaT cells expressed high levels of exhaustion ligands and thereby negated adaptive anti-tum

168 iral Ag in infected lungs rapidly induces an exhaustion-like state in lung TCD8 characterized by prog

169 ndritic cells and prevention of aberrant and exhaustion-like T-cell phenotypes.

170 Functional exhaustion limits effector CD4(+) and CD8(+) T-lymphocyt

171 lty-related phenotype criteria (weight loss, exhaustion, low activity, slowness) at >/=2 visits, or a

172 he following: low muscle mass, self-reported exhaustion, low energy expenditure, slow walking speed,

173 ing characteristics: clinically underweight, exhaustion, low energy expenditure, slow walking speed,

174 he baseline consumption of fruit and risk of exhaustion, low physical activity, and slow walking spee

175 We measured frailty (shrinking, weakness, exhaustion, low physical activity, and slowed walking sp

176 n preceded the overt establishment of T cell exhaustion, making this signature a prime target in the

177 LAG3 expression, contributing to a state of exhaustion manifest in impaired proliferation and cytoki

178 mice with B. melitensis led to CD8(+) T cell exhaustion, manifested by programmed cell death 1 (PD-1)

179 tion, equal differentiation, senescence, and exhaustion marker expression and were negative for regul

180 V-driven immune activation, decreased T cell exhaustion marker expression, restored HIV-specific CD8

181 n between expression of CD39, a novel immune exhaustion marker, and early mortality in patients with

182 h1/Th17-type phenotype; (3) depressed T cell exhaustion markers (PD-1, LAG3); and (4) elevated neutro

183 ponding increase in the expression of T-cell exhaustion markers and tumor-promoting cytokines.

184 These data indicate that T-cell exhaustion markers may identify those latently infected

185 including their signature high expression of exhaustion markers PD-1 and CD39.

186 otype characterized by downregulation of the exhaustion markers PD-1 and LAG-3.

187 T-cell exhaustion markers PD-1, Tim-3 and Lag-3 measured prior

188 cl-2, whereas it dampened the display of the exhaustion markers programmed death receptor 1 (PD-1) an

189 receptor PD-1, suggesting that induction of exhaustion may be a therapeutic strategy in autoimmune a

190 Conversely, its exhaustion may contribute to the irreversible disability

191 sing or encouraging the natural processes of exhaustion may provide a novel means to promote graft su

192 1 expression in mediating CD4 and CD8 T cell exhaustion may provide a rational basis for designing no

193 protein levels, and propose a T helper cell exhaustion model resembling that of stem cell exhaustion

194 sfunction, as marked by expression of T cell exhaustion molecules, and posttransplant infections in a

195 4, highlighting mechanical variables in the exhaustion occurrence and even training prescription app

196 The extent of T cell exhaustion occurring with various allografts, the kineti

197 This phenotype, known as T cell exhaustion, occurs during chronic infections caused by a

198 nd LAG-3 on T cells contributes to the rapid exhaustion of A. marginale-specific T cells following in

199 quently dysfunctional, which can cause rapid exhaustion of anti-tumor immune responses.

200 However, the infection induces a functional exhaustion of antigen-specific CD4(+) T cells in cattle

201 Exhaustion of antiviral CD8(+) T cells contributes to pe

202 e-chain variable fragments, can induce early exhaustion of CAR T cells that limits antitumor efficacy

203 ns that impact persistence and resistance to exhaustion of CAR-T cells remain largely undefined.

204 its isohydric strategy pushes it towards the exhaustion of carbon reserves during much of the growing

205 with the accumulation of a CD62L+ subset and exhaustion of CD62L- cells.

206 n squamous cell carcinoma (SCC) cells drives exhaustion of CD8(+) T cells and recruitment of regulato

207 Exhaustion of CD8(+) T cells severely impedes the adapti

208 Exhaustion of chronically stimulated CD8(+) T cells is a

209 Loss of Bcl11b leads to a Cdkn2a-dependent exhaustion of ductal epithelium and loss of epithelial c

210 n of magnetite to siderite, coupled with the exhaustion of ferrihydrite.

211 ing that leads to the expansion and eventual exhaustion of hematopoietic cells, and this occurs in th

212 In absence of WDR47, the exhaustion of late cortical progenitors and the conseque

213 aling that BMP signaling inactivation causes exhaustion of lipid reserves in somatic tissues.

214 arily against nonconserved class I epitopes; exhaustion of liver-infiltrating CD8(+) T cells that tar

215 5-fluorouracil (5-FU) and, in turn, induces exhaustion of long-term HSC function along serial bone m

216 Exhaustion of lymphocyte function through chronic exposu

217 HMGB1-RAGE signaling resulted in functional exhaustion of mature monocytes and lymphopenia, the hall

218 ation for the previously reported functional exhaustion of NK cells after allogeneic HSCT and suggest

219 Disrupted tumor blood vessels promote exhaustion of non-malignant stem and progenitor cells an

220 c changes, deregulated nutrient sensing, and exhaustion of progenitor cells.

221 in conditions of HO-1 deficiency may lead to exhaustion of SC pool, and the number of SCs is decrease

222 ight, indicating that it is due to premature exhaustion of starch.

223 ue to intensive lifestyle intervention) and "exhaustion of susceptible" (changes in mean genetic and

224 Results were consistent with exhaustion of susceptibles for the change in incidence r

225 ic risk score over time were consistent with exhaustion of susceptibles.

226 ent membrane, led to ESC mislocalization and exhaustion of the ESC pool.

227 at meth users have greater proliferation and exhaustion of the immune system.

228 ender dependent and not due to proliferative exhaustion of the incumbent embryonic population, despit

229 Here, we show that exhaustion of the metabolic inputs that couple carbon ca

230 the ASPM locus, and demonstrate a premature exhaustion of the neuronal progenitor pool due to dysfun

231 al months was not accompanied by accelerated exhaustion of the neuronal stem cell (NSC) reserve, ther

232 hat distracts cell division mode, leading to exhaustion of the progenitor pool.

233 results are consistent with a model in which exhaustion of the proliferative capacity of naive T cell

234 chronic inflammatory response leading to the exhaustion of the resident T cells in the EP.

235 notype could not expand in vitro, suggesting exhaustion of these cells.

236 cular SCs in mice lacking CTIP2 leads to the exhaustion of this SC compartment in comparison with Cti

237 ranscriptome studies were consistent with an exhaustion of unknown primary phosphorus-storage molecul

238 hallmarks of persistent viral infections are exhaustion of virus-specific T cells, elevated productio

239 C virus (HCV) infection is characterized by exhaustion of virus-specific T-cells and stable viremia.

240 of type I interferons, progressive loss (or exhaustion) of CD8(+) T cell functions, and specializati

241 ferent immunosuppressants, and the impact of exhaustion on graft survival and tolerance development r

242 ic CD4(+) T cells did not display defects in exhaustion or polyfunctionality compared with healthy HI

243 ing levels of cells indicating either T-cell exhaustion or systemic immunosuppression may be markers

244 T cell expansion without increasing anergy, exhaustion, or apoptosis, resulting in strong GVL effect

245 ts rendered senescent by stress, replicative exhaustion, or oncogene activation, mTORC1 is constituti

246 fter 5-FU treatment, and this results in HSC exhaustion over time.

247 ed with the core burnout dimension emotional exhaustion (p </= 0.001), which significantly mediated t

248 Low energy expenditure (p = 0.03), exhaustion (p = 0.01), and slow gait speed (p = 0.03) we

249 ugh the programmed cell death protein (PD)-1 exhaustion pathway were investigated as a potential key

250 activation (CD45RA(-)CD38(+), p = 0.005) and exhaustion (PD-1(+), p = 0.0004) in blood, compared to n

251 i67; 15.10% vs 26.80%; P = .016), and immune exhaustion (PD-1; 32.45% vs 40.00%; P = .005) in 243 ant

252 Cellular senescence occurs by proliferative exhaustion (PEsen) or following multiple cellular stress

253 -onset sepsis and nonsurvivors had an immune exhaustion phenotype, which may represent one of the mai

254 r mechanism by itself could fully rescue the exhaustion phenotype.

255 ptors have been connected to the immune cell exhaustion phenotype; furthermore, ligands capable of ac

256 we review the molecular regulation of T cell exhaustion, placing recent findings on PD-1 blockade the

257 Thus, T-cell exhaustion plays a central role in determining outcome i

258 lysis of tumor-infiltrating T cells revealed exhaustion programs, their connection to T cell activati

259 markers of inflammation; T-cell activation, exhaustion, proliferation; and innate cellular subsets a

260 h correlated with expression of a variety of exhaustion-related inhibitory markers.

261 >/=3 of the following 5 criteria: shrinking, exhaustion, sedentariness, slowness, and weakness.

262 Its expression correlates with exhaustion severity and identifies terminally exhausted

263 f CD4(+) T cells following P. yoelii-induced exhaustion shows upregulation of effector T cell-associa

264 le from 0 to 5 by grip strength, gait speed, exhaustion, shrinkage, and physical activity, with score

265 We can reproduce the exhaustion signature by modifying the balance of persist

266 Second, CYM-5442 induced an exhaustion signature in antiself T cells by up-regulatin

267 optimal surrogate markers of co-stimulation/exhaustion signatures in independent data sets, we confi

268 ar whether elite controllers manifest T-cell exhaustion similar to subjects with chronic progression

269 Exhaustion-specific accessible regions were enriched for

270 t PD-1 expression is regulated in part by an exhaustion-specific enhancer that contains essential RAR

271 cific murine CD8 T cells at the effector and exhaustion stages of an immune response identified progr

272 es tumor immune evasion and modulates T cell exhaustion state towards memory and effector T cell phen

273 dy, we assessed the frequency, function, and exhaustion status of TG-resident CD8(+)T cells specific

274 0% showed evidence of severe burnout on the "exhaustion" subscale, 44% on the "depersonalization" sub

275 and reduced lifespan, and of virus-specific exhaustion, such as CD21(low) phenotype and a defective

276 h high CD39 expression exhibited features of exhaustion, such as reduced production of TNF and IL2 an

277 s, and parameters associated with lymphocyte exhaustion/suppression showed higher clinical significan

278 herefore more resistant to P. yoelii-induced exhaustion than their wild-type counterparts.

279 Leukemia can promote T cell dysfunction and exhaustion that contributes to increased susceptibility

280 XCR4 and PD-1 (PDCD1), a regulator of T-cell exhaustion that is a validated target for tumor immunoth

281 review, we describe basic concepts of T-cell exhaustion that occur in cancer, highlighting the role o

282 understanding of the molecular regulation of exhaustion, the cytokines that directly control this pro

283 utilization (GAL) genes hours before glucose exhaustion, thereby "preparing" for the transition from

284 asis and to prevent apoptotic and functional exhaustion, thereby orchestrating the balance between im

285 ant work rate (CWR) tests slightly >CP until exhaustion (Tlim ), slightly <CP for 24 min and until th

286 Addition of PD-L1 blockade reverses T-cell exhaustion to mitigate depression in the CD8/Treg ratio

287 xhaustion model resembling that of stem cell exhaustion to understand decline in T cell-dependent hum

288 pleted four constant power handgrip tests to exhaustion under conditions of control exercise (Con), b

289 l failure in HCV infection, including T-cell exhaustion, viral escape, and functional impairment of n

290 This reversal of CD8(+) T-cell exhaustion was dependent on both agonistic GITR signalin

291 rison to senior physicians), while emotional exhaustion was highest in junior physicians (p </= 0.015

292 prisingly, the content of muscle acyl-CoA at exhaustion was markedly elevated, indicating that acyl-C

293 Immune exhaustion was studied in subcohort of 103 patients.

294 re, Tim-3, an indicator of activation and/or exhaustion, was upregulated 3-fold on LN NK cells in chr

295 xpression might represent a marker of T-cell exhaustion; we hypothesised that expression could predic

296 ecrease in effector function, referred to as exhaustion, which impairs responses in the setting of tu

297 onic presence of viral Ags can induce T cell exhaustion, which is characterized by upregulation of co

298 fic CD8(+) T cell effector function, termed "exhaustion," which is mediated, in part, by the membrane

299 Reversing immune exhaustion with an anti-PD-L1 antibody may improve human

300 grammed death-1 (PD-1) pathway in CAR T cell exhaustion within the tumor microenvironment, and demons