ライフサイエンスコーパス: cell dysfunction

1 s tolerant phenotypes that promoted CD8(+) T cell dysfunction.

2 2.4% (11.2-13.7) could be attributed to beta-cell dysfunction.

3 ow PII component, suggesting specific Muller cell dysfunction.

4 m contributing to glucotoxicity-induced beta-cell dysfunction.

5 elios, and other molecules associated with T cell dysfunction.

6 atting autoimmune diseases mediated by T reg cell dysfunction.

7 islet inflammation develops and causes beta cell dysfunction.

8 ing in enhanced PD-1 expression and CD4(+) T cell dysfunction.

9 tic patients before they develop severe beta cell dysfunction.

10 vating mutation in STAT3 and pancreatic beta-cell dysfunction.

11 of lung diseases characterized by epithelial cell dysfunction.

12 d the epigenetic landscape associated with T-cell dysfunction.

13 echanism of HHcy induced retinal endothelial cell dysfunction.

14 ion induces a sustained vascular endothelial cell dysfunction.

15 art immune responses in humans by inducing T cell dysfunction.

16 abolic insufficiency can imprint permanent T cell dysfunction.

17 conducive to tumor progression and further T cell dysfunction.

18 istance, hyperglycemia, and progressive beta cell dysfunction.

19 ps, indicating a higher grade of endothelial cell dysfunction.

20 tion that can be targeted to ameliorate beta cell dysfunction.

21 hepatitis B virus (HBV) is associated with T cell dysfunction.

22 c targets to prevent amyloid-associated beta cell dysfunction.

23 d a modest therapeutic effect resulting from cell dysfunction.

24 to capture the early pathophysiology of beta cell dysfunction.

25 C1 signaling and glucose metabolism drives T cell dysfunction.

26 order to identify factors predictive of beta cell dysfunction.

27 from peripheral insulin resistance and beta-cell dysfunction.

28 us candidiasis, which are suggestive of TH17 cell dysfunction.

29 PD1, TIM3, LAG3, and TIGIT, resulting in TFH cell dysfunction.

30 ary diseases that result primarily from ATII cell dysfunction.

31 lockade of this pathway partially reverses T cell dysfunction.

32 d that are instructive to understand naive T cell dysfunction.

33 esponses via induction of Tim-3, IL-10 and T-cell dysfunction.

34 irmed the direct implication of IGF2 on beta-cell dysfunction.

35 eveloped to treat IBD patients with CD8(+) T cell dysfunction.

36 etes are now believed to be preceded by beta-cell dysfunction.

37 r together with PD-1, is not indicative of T cell dysfunction.

38 phages to IAPP-induced inflammation and beta-cell dysfunction.

39 esulted in some reversal of retinal ganglion cell dysfunction.

40 versing age-related skeletal muscle and stem cell dysfunction.

41 hronic infections; and (iii) tumor-induced T cell dysfunction.

42 withdrawal without evidence of regulatory T cell dysfunction.

43 re exerting their disease risk through islet-cell dysfunction.

44 te early metabolic events leading up to beta-cell dysfunction.

45 hat the HPK1-NFkappaB-Blimp1 axis mediates T cell dysfunction.

46 bolism, and both adipose and pancreatic beta-cell dysfunction.

47 to type 2 diabetes is primarily due to beta-cell dysfunction.

48 on in beta-cells lacking Furin, causing beta-cell dysfunction.

49 ycemic conditions and monitoring endothelial cell dysfunction.

50 graft removal precluded the acquisition of T cell dysfunction.

51 and show impaired glucose tolerance and beta-cell dysfunction.

52 CD8(+) and CD4(+) T cells, indicative for T-cell dysfunction.

53 es induced human coronary artery endothelial cells dysfunction.

54 ance of negative co-stimulation results in T cell dysfunction(2).

55 beta cells in response to HDF-mediated beta cell dysfunction, a novel finding.

56 rated a mixed transcriptional signature of T cell dysfunction, activation, and effector function.

57 form to longitudinally examine patterns of T-cell dysfunction alongside developing CLL and in differe

58 h implications for defining a biomarker of T-cell dysfunction and a target for immunotherapeutic inte

59 es, altered redox balance can cause vascular cell dysfunction and affect the equilibrium between proc

60 Islet beta-cell dysfunction and aggressive macrophage activity are

61 we demonstrate that HPK1 is a mediator of T cell dysfunction and an attractive druggable target to i

62 tic islets reduced cytokines, prevented beta-cell dysfunction and apoptosis and reduced recruiting of

63 At a cellular level, stem cell dysfunction and attrition appear to be key events,

64 exploit existing models to understand immune cell dysfunction and break the devastating relationship

65 accumulation in nonadipose tissues leads to cell dysfunction and cell death that is linked to the pa

66 their persistent expression often leads to T cell dysfunction and compromised protective immunity.

67 stress is thought to promote pancreatic beta-cell dysfunction and contribute to both type 1 and type

68 direct involvement in antibody-mediated beta-cell dysfunction and cytotoxicity.

69 s-mediated pancreatic insulin-producing beta-cell dysfunction and death are critical elements in the

70 Conjunctival goblet cell dysfunction and death are promoted by the T helper

71 The pathogenic mechanism resulting in cell dysfunction and death beyond the causative mutation

72 s the evidence for a role of the UPR in beta-cell dysfunction and death in the development of type 2

73 le of inflammation in cytokine-mediated beta-cell dysfunction and death in type 1 diabetes mellitus,

74 mately associated with pancreatic islet beta-cell dysfunction and death in type II diabetes.

75 ons in sphingolipid metabolism contribute to cell dysfunction and death.

76 process which contributes to pancreatic beta-cell dysfunction and death.

77 bility genes for diabetes contribute to beta cell dysfunction and death.

78 (IAPP) misfolding, a process central to beta-cell dysfunction and death.

79 beta-Cell dysfunction and declining beta-cell mass are two me

80 tter being a protein strongly linked to beta-cell dysfunction and diabetes.

81 2 diabetes, may therefore contribute to beta-cell dysfunction and disease progression.

82 Disrupted energy metabolism drives cell dysfunction and disease, but approaches to increase

83 mechanisms differentially affect early beta-cell dysfunction and eventual fate.

84 ervations and validated the correlation of T cell dysfunction and exclusion programs with resistance.

85 evealed strong associations with cytotoxic T-cell dysfunction and exclusion, respectively.

86 Leukemia can promote T cell dysfunction and exhaustion that contributes to incr

87 olonged in the hemizygous mice, wherein beta-cell dysfunction and extensive oligomer formation occurr

88 1beta action by IL-1betaAb counteracted beta-cell dysfunction and glucose intolerance, supporting the

89 et 12/15-LOX can prevent progression of beta-cell dysfunction and glycemic deterioration in models of

90 and lacked startle response, indicating hair cell dysfunction and gross hearing impairment.

91 APIs may be predisposed to pancreatic beta-cell dysfunction and have the highest prevalence of gest

92 the bidirectionality of obesity-induced stem cell dysfunction and how the molecular changes in stem c

93 ing cell contact-dependent brain endothelial cell dysfunction and increased barrier permeability in a

94 ed to promote pulmonary arterial endothelial cell dysfunction and induce pulmonary arterial smooth mu

95 n, and proliferation, as well as endothelial cell dysfunction and inflammation.

96 The hyperglycaemia results from beta-cell dysfunction and is associated with lower fasting an

97 ted in progressive establishment of CD4(+) T cell dysfunction and long-term allograft survival.

98 lum (ER) stress, which is implicated in beta-cell dysfunction and loss during the pathogenesis of typ

99 ent activation is strongly implicated in RPE cell dysfunction and loss in age-related macular degener

100 is causally associated with pancreatic beta-cell dysfunction and loss of pancreatic insulin.

101 pe 2 diabetes (T2D) is characterized by beta cell dysfunction and loss.

102 ids and lipid peroxides that exacerbate beta-cell dysfunction and macrophage activity.

103 ic knowledge advances our understanding of T cell dysfunction and may lead to novel approaches that e

104 We highlight muscle progenitor cell dysfunction and metabolism as two variables contrib

105 ressive cerebellar ataxia linked to Purkinje cell dysfunction and mild exercise intolerance, recapitu

106 2 diabetes mellitus (T2DM), the role of beta-cell dysfunction and peripheral insulin resistance (IR)

107 lic disease characterized by pancreatic beta-cell dysfunction and peripheral insulin resistance.

108 beta-Cell dysfunction and reduction in beta-cell mass are hal

109 Understanding the effects of HIV on B cell dysfunction and restoration following ART may provi

110 intrinsic deletion of Blimp-1 reversed CD8 T cell dysfunction and resulted in improved pathogen contr

111 This was associated with extensive nerve cell dysfunction and severe paralysis by the age of 3 we

112 factors and epigenetic programs underlying T cell dysfunction and surface markers that predict therap

113 ive form of STAT5 partially ameliorates Treg cell dysfunction and systemic inflammation in O-GlcNAc d

114 immune response, mainly characterized by NK cell dysfunction and T cell exhaustion.

115 onsistently generate data showing islet beta-cell dysfunction and T cell-mediated anti-beta-cell-spec

116 a new therapeutic strategy to diminish beta-cell dysfunction and the development of T2D.

117 tical factor for the normal progression of T cell dysfunction and the maintenance of exhausted T cell

118 allmark of many cancers, but the basis for T cell dysfunction and the mechanisms by which antibody bl

119 Endothelial cell dysfunction and the proteolytic disorganization of

120 imary role of Chop in tumor-induced CD8(+) T cell dysfunction and the therapeutic potential of blocki

121 The epigenetic regulation of T cell dysfunction and therapeutic reprogrammability (for

122 pathway, has a strong association with beta-cell dysfunction and type 2 diabetes through a mechanism

123 ve disease characterized by lung endothelial cell dysfunction and vascular remodeling.

124 Neural precursor cell dysfunction and white matter dysfunction are though

125 he loss of insulin production caused by beta-cell dysfunction and/or destruction.

126 key general regulator in the induction of T cell dysfunction, and a potential target for tumour immu

127 ing Th17 cell-associated cytokines, CD8(+) T cell dysfunction, and alterations of B cell and innate i

128 haracterized by poor prognosis, markers of T cell dysfunction, and alternatively activated macrophage

129 sue pathology, including inflammation, glial cell dysfunction, and angiogenesis, its role in the reti

130 but not separately to achieve alloreactive T cell dysfunction, and conventional immunosuppression cou

131 athways involved in insulin resistance, beta-cell dysfunction, and inflammation, but human studies ar

132 bsequent adiposity, insulin resistance, beta-cell dysfunction, and metabolic syndrome, leading to car

133 the interaction of insulin resistance, beta-cell dysfunction, and obesity with the development of di

134 ntrols a core regulatory circuit of CD4(+) T cell dysfunction, and targeting IRF4 represents a potent

135 pathogenic variant display progressive hair cell dysfunction, and that CLRN1(N48K) is trafficked to

136 ty acids have in insulin resistance and beta-cell dysfunction, and the potential role of changes in t

137 within cells, it generates variously severe cell dysfunctions, and even cell death.

138 directly or indirectly contribute to these B cell dysfunctions, and one of these is the B cell-activa

139 es to the clinical assessment of endothelial cell dysfunction; and outline some promising new directi

140 Both insulin resistance and beta-cell dysfunction are generally agreed to contribute to d

141 They further identify beta-cell dysfunction as a potential therapeutic target in pe

142 tes mellitus (T2DM) is characterized by beta-cell dysfunction as a result of impaired glucose-stimula

143 afish show remarkable conservation of immune cell dysfunction as found in mice and humans and will se

144 with T2D were largely mediated through beta-cell dysfunction, as indicated by HOMA-B (mediation prop

145 this study, we examined the association of T cell dysfunction, as marked by expression of T cell exha

146 microbiome dysbiosis might promote CD4(+) T cell dysfunction associated with childhood atopy.

147 effectively reversing the persistent immune cell dysfunction associated with long-term sepsis mortal

148 SIV-associated B cell dysfunction associated with the pathogenic SIV infe

149 nterrogated the molecular mechanisms of beta-cell dysfunction at the level of mRNA translation under

150 AFF, a phenomenon that might contribute to B cell dysfunctions at inflammatory tissue sites in infect

151 e specific antibody responses secondary to T cell dysfunction, but B cells have not been shown to be

152 oxO1 is involved in the pathogenesis of beta cell dysfunction, but its link to human diabetes GWAS ha

153 er, chronically elevated glucose causes beta-cell dysfunction, but little is known about how cells ha

154 MHCII complexes from DCs and induce CD4(+) T cell dysfunction by presenting transferred complexes to

155 tidase CD39 in TAMs, which promotes CD8(+) T cell dysfunction by producing adenosine in cooperation w

156 gression of arterial plaques and endothelial cell dysfunction, CAD is commonly viewed as a chronic in

157 to mousepox, these data suggest that the NK cell dysfunction caused by CL13 persistence may contribu

158 BACKGROUND & AIMS: Paneth cell dysfunction causes deficiencies in intestinal C-typ

159 red type I interferon (IFN) responses, and B cell dysfunctions causing susceptibility to opportunisti

160 emia in these patients is an outcome of beta-cell dysfunction consequent to GIP resistance and hyperg

161 Insulin resistance and beta cell dysfunction contribute to the pathogenesis of type

162 Inflammation, ischemia, and glial cell dysfunction contribute to this persistent brain inj

163 Alveolar type II (AT2) cell dysfunction contributes to a number of significant

164 Pancreatic beta-cell dysfunction contributes to onset and progression of

165 player in the progression of pancreatic beta-cell dysfunction contributing to insulin resistance and

166 The observation that the degree of beta cell dysfunction correlates with the severity of MetS hi

167 the nutrient surplus ensues, leading to beta-cell dysfunction, dedifferentiation, and apoptosis.

168 eads to excessive workload resulting in beta-cell dysfunction, dedifferentiation, death, and developm

169 We report here that the HIV/SIV-associated B cell dysfunction (defined by loss of total and memory B

170 e range of evidence implicating HIFs in beta cell dysfunction, diabetes pathogenesis, and diabetes co

171 Although SIV infection resulted in NK cell dysfunction, double-negative NK cells and those exp

172 The likely mechanism is endothelial cell dysfunction due to increased MEK1 activity.

173 n be difficult as patients frequently have T-cell dysfunction, due to disease and/or treatment-relate

174 ng the first immunologic evidence of CD8(+)T cell dysfunction during acute infection.

175 expression of several proteins related to T cell dysfunction during chronic infection.

176 hibitory receptor that has a major role in T cell dysfunction during chronic infections and cancer.

177 is a major inhibitory receptor regulating T cell dysfunction during chronic viral infection and canc

178 buildup and less lung epithelial/endothelial cell dysfunction (edema and hemorrhage).

179 the evolution of the concept of endothelial cell dysfunction, focusing on recent insights into the c

180 Although beta-cell dysfunction has a clear genetic component, environm

181 e defense mechanism against infection, and B cell dysfunction has been implicated in pregnancy compli

182 Satellite cell dysfunction has been shown to underlie the loss of

183 Epithelial cell dysfunction has emerged as a central component of t

184 2 diabetes (T2D) and its involvement in beta cell dysfunction has further highlighted the significanc

185 In addition to causing NK cell dysfunction, HIV-1 infection contributes to the exp

186 MA of insulin resistance [HOMA-IR]) and beta-cell dysfunction (HOMA of beta-cell function [HOMA-B]) t

187 munodeficiency that has been attributed to T cell dysfunction; however, any contribution of B cells i

188 ronic lymphocytic leukemia (CLL), acquired T-cell dysfunction impedes development of effective immuno

189 mediated by insulin resistance (IR) and beta-cell dysfunction in a population-based cross sectional s

190 Considering prior studies of intrinsic PV cell dysfunction in AD, these findings suggest alteratio

191 evelopmental programming predisposes to beta-cell dysfunction in adults and raise questions on the de

192 Identifying factors driving neural stem cell dysfunction in age-related neurodegenerative diseas

193 vel insights in the modulation of epithelial cell dysfunction in asthma.

194 T cell dysfunction in cancer comes in many forms, with two

195 f AMPK inhibitors to overcome MDSC-induced T-cell dysfunction in cancer.

196 onversion in wound healing and smooth muscle cell dysfunction in cardiac disease.

197 iation with incident diabetes than does beta-cell dysfunction in Chinese adults, and this association

198 n the search for the regulatory origins of T cell dysfunction in chronic viral infection.

199 transduction and attenuated progressive hair cell dysfunction in clrn1 (KO/KO) larvae that express CL

200 endocytosis are paramount to pancreatic beta cell dysfunction in diabetes mellitus.

201 beta-Cell dysfunction in diabetes results from abnormalities

202 ay contribute to beta cell failure and alpha cell dysfunction in diabetes.

203 ls and thereby may contribute to endothelial cell dysfunction in diabetic vascular disease where tRES

204 sis and lipid oxidation, accompanied by beta-cell dysfunction in fat and glucose metabolism, enhancin

205 pite evidence of insulin resistance and beta-cell dysfunction in glucose metabolism in youth with pre

206 how metabolism may be targeted to prevent T cell dysfunction in inhospitable microenvironments, to g

207 ta, a syndrome characterized by somatic stem cell dysfunction in multiple organs leading to BM failur

208 ibitory immune receptors can contribute to T cell dysfunction in patients with cancer(1,2).

209 M-MDSCs and G-MDSCs strongly contribute to T-cell dysfunction in patients with sepsis.

210 g are emerging as important features of beta cell dysfunction in patients with type 1 and type 2 diab

211 ine the molecular foundation of pathogenic B cell dysfunction in SLE.

212 T cell dysfunction in solid tumors results from multiple m

213 a or insulin resistance, and shows that beta-cell dysfunction in T2D can be explained by an impaired

214 s may contribute to LD accumulation and beta cell dysfunction in T2D islets.

215 s may contribute to LD accumulation and beta-cell dysfunction in T2D islets.

216 urthermore, the mechanisms underpinning beta-cell dysfunction in T2D remain undetermined.

217 ave previously demonstrated tumor-specific T-cell dysfunction in the allogeneic environment.

218 ighlights the need to better understand beta cell dysfunction in the development of MetS.

219 de new insights into the nature of pyramidal cell dysfunction in the illness.

220 ed in insulin resistance and pancreatic beta cell dysfunction in the metabolic syndrome.

221 ng anti-tumor immunity and contributing to T cell dysfunction in the tumor microenvironment.

222 icv FGF1 injection delays the onset of beta-cell dysfunction in these animals, it has no effect on e

223 o studies have investigated the role of beta-cell dysfunction in type 2 diabetes (T2D), whereas in vi

224 yloid polypeptide (IAPP) contributes to beta cell dysfunction in type 2 diabetes and islet transplant

225 Glucotoxicity-induced beta-cell dysfunction in type 2 diabetes is associated with a

226 rol Ca(2+) handling and how they impact beta-cell dysfunction in type 2 diabetes.

227 lay an important role in stress-induced beta-cell dysfunction in type 2 diabetes.

228 transmission could contribute to endothelial cell dysfunction in various pathologies.

229 uman beta-cells from tacrolimus-induced beta-cell dysfunction in vitro.

230 and delays accelerated aging, including stem cell dysfunction, in Caenorhabditis elegans and Drosophi

231 incident T2D, largely mediated through beta-cell dysfunction, in Chinese individuals.

232 Endothelial cell dysfunction, in its broadest sense, encompasses a c

233 ontrolling protein synthesis can result in T-cell dysfunction, indicating a mechanism by which mTORC1

234 of mitochondrial ROS overproduction as lung cells' dysfunctions induced by the virus.

235 This stem cell dysfunction induces a significant delay in recovery

236 ic factors, and that amacrine and horizontal cell dysfunction induces alterations to the intraretinal

237 Established T cell dysfunction is a barrier to antitumor responses, an

238 T cell dysfunction is a characteristic feature of chronic

239 beta-Cell dysfunction is a common contributor to the pathogen

240 Tumour-specific CD8 T cell dysfunction is a differentiation state that is dist

241 T cell dysfunction is a hallmark of many cancers, but the

242 ogether, these findings indicate that goblet cell dysfunction is an epithelial-autonomous defect in t

243 beta-Cell dysfunction is central to the pathogenesis of impai

244 by which RPGR mutations cause photoreceptor cell dysfunction is not well understood.

245 Endothelial cell dysfunction is pivotal to the pathophysiology, but

246 T cell dysfunction is well documented during chronic viral

247 actors for Leydig cell failure (LCF), Leydig cell dysfunction (LCD), and associated adverse health ou

248 ted that LAMP3 expression induces epithelial cell dysfunction leading to apoptosis.

249 However, the mechanism(s) underlying beta-cell dysfunction leading to hyperproinsulinemia is poorl

250 Fibrosis can be initiated by an epithelial cell dysfunction, leading to low-grade inflammation, mac

251 nset of viremia mitigates peripheral T and B cell dysfunction, limits seroconversion, and enhances ce

252 , implicating loci linked to pancreatic beta cell dysfunction, lipid dysregulation and insulin resist

253 of tumor recognition, clonal expansion and T cell dysfunction marked by clonal expansion of CD8(+)CD3

254 Vascular endothelial cell dysfunction mediated by antiphospholipid antibodies

255 BV persists with virus-specific and global T-cell dysfunction mediated by multiple regulatory mechani

256 d suppressive function, indicating that Treg cell dysfunction might be a key contributor to disease p

257 fections to assess the significance of the B cell dysfunction observed in simian (SIV) and human immu

258 Skeletal muscle atrophy and endothelial cell dysfunction occur in tandem in cardiovascular disea

259 Endothelial and satellite cell dysfunction occur in tandem in many disease states;

260 Important comorbidities caused by epithelial cell dysfunction occur in the pancreas (malabsorption),

261 Since beta cell dysfunction occurs during diabetes development, it

262 In models of melanoma cancer in which T cell dysfunction occurs, PSGL-1 deficiency led to PD-1 d

263 model to understand the relationship between cell dysfunction, parainflammation, liver fibrosis, and

264 cells, and be taken up without inducing ATII cell dysfunction, pulmonary inflammation, lung damage, o

265 g interleukin-6 levels), reduced endothelial cell dysfunction (reduced endothelial activation and cir

266 Unlike insulin resistance, beta cell dysfunction remains difficult to predict and monito

267 implication in glucotoxicity-associated beta-cell dysfunction remains to be defined.

268 ssociated with endothelial and smooth muscle cell dysfunction, rescued by enzastaurin through a dual

269 Impaired insulin sensitivity (IS) and beta-cell dysfunction result in hyperglycaemia in patients of

270 Thus, T cell dysfunction seen in advanced human cancers may alre

271 B cell dysfunction should be considered in designing immun

272 Despite of the B cell dysfunction, SIV-specific antibody (Ab) production

273 and molecular analysis identified mutant BM cell dysfunction suggestive of a PAH phenotype soon afte

274 ew, we propose a central role for epithelial cell dysfunction that accounts for the dual role of skin

275 ons to identify a distinct gene module for T cell dysfunction that can be uncoupled from T cell activ

276 has emerged as a critical regulator of the T-cell dysfunction that develops in chronic viral infectio

277 ons are characterized by a state of CD8(+) T-cell dysfunction that is associated with expression of t

278 defining and reversing the persistent immune cell dysfunction that is associated with mortality long

279 immunosenescence is an important state of T cell dysfunction that is distinct from exhaustion, a key

280 se results inform on the mechanism of goblet cell dysfunction that underlies the pathology of ulcerat

281 etes and ask the following question: Is beta-cell dysfunction the result of a maladaptive UPR or a fa

282 ular pathogenic pathways secondary to Muller cell dysfunction, the cause of which remains obscure, ex

283 gate measures of insulin resistance and beta-cell dysfunction, these findings should be interpreted w

284 Different from T cell dysfunction, this FRC-mediated suppression is surmo

285 flexibility, initiates progression from beta-cell dysfunction to beta-cell dedifferentiation.

286 4 may protect against cytokine-mediated beta-cell dysfunction to insulin secretion dynamics during th

287 s as an important nexus linking primary beta-cell dysfunction to progressive beta-cell mass deteriora

288 endent kinase 2 (CDK2), couples primary beta-cell dysfunction to the progressive deterioration of bet

289 hogenesis of the most prevalent form of beta cell dysfunction, type 2 diabetes.

290 other circular RNAs helps understanding beta-cell dysfunction under diabetes conditions, and the etio

291 ta-cells will confer protection against beta-cell dysfunction under diabetogenic conditions.

292 highlighting that other aspects of Purkinje cell dysfunction underpin the pathogenic loss of GLAST.

293 dy investigated how induction of endothelial cell dysfunction via high glucose treatment impacts grow

294 Dasatinib treatment mediated endothelial cell dysfunction via increased production of ROS that wa

295 lipid exposure is associated with islet beta-cell dysfunction, we investigated LD accumulation in the

296 glycemic dysregulations and pancreatic beta-cell dysfunctions, we evaluated islet function and gluco

297 aging, tumor progression and PD-1-mediated T cell dysfunction which is driven, at least in part, by l

298 the mutation may be caused by cochlear hair cells dysfunction, which manifests with shortening and f

299 ) showed impaired islet vasculature and beta-cell dysfunction, while restoring c-Kit expression in be

300 associations of insulin resistance and beta-cell dysfunction with incident diabetes, and to examine

301 Here, we discuss distinct states of CD8 T cell dysfunction, with an emphasis on: (i) T cell tolera