ライフサイエンスコーパス: cell dysfunction

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

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

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

4 d a modest therapeutic effect resulting from cell dysfunction.

5 to capture the early pathophysiology of beta cell dysfunction.

6 C1 signaling and glucose metabolism drives T cell dysfunction.

7 order to identify factors predictive of beta cell dysfunction.

8 from peripheral insulin resistance and beta-cell dysfunction.

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

10 ary diseases that result primarily from ATII cell dysfunction.

11 lockade of this pathway partially reverses T cell dysfunction.

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

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

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

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

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

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

18 esulted in some reversal of retinal ganglion cell dysfunction.

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

20 atting autoimmune diseases mediated by T reg cell dysfunction.

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

22 leukemia (CLL), on a background of global T-cell dysfunction.

23 2D) results from insulin resistance and beta cell dysfunction.

24 irectly measured insulin resistance and beta-cell dysfunction.

25 islet inflammation develops and causes beta cell dysfunction.

26 SLs restored TCR signaling and ameliorated T cell dysfunction.

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

28 ing disorders of insulin resistance and beta-cell dysfunction.

29 roteins (TGRLs) might cause pancreatic alpha cell dysfunction.

30 with DM preceded predominantly by IR or beta-cell dysfunction.

31 s contributed directly to HIV-1-associated B cell dysfunction.

32 velopment of diabetes and contribute to beta-cell dysfunction.

33 ts in GATA2 are a novel cause of profound NK cell dysfunction.

34 d smoking, and is thus a marker of bronchial cell dysfunction.

35 e not well regulated and produce endothelial cell dysfunction.

36 istent with a joint signature of IR and beta-cell dysfunction.

37 ads to glucose intolerance secondary to beta-cell dysfunction.

38 us is a rare genetic form of pancreatic beta-cell dysfunction.

39 ine hypomorphic (HM) activity, causes Paneth cell dysfunction.

40 tained PD-1 expression plays a key role in T cell dysfunction.

41 ssue insulin resistance; and pancreatic beta cell dysfunction.

42 ession of gene products associated with beta-cell dysfunction.

43 tic patients before they develop severe beta cell dysfunction.

44 ired T cell-dependent B-cell responses and T-cell dysfunction.

45 sis on the role of neural stem and precursor cell dysfunction.

46 ave previously been associated with memory B-cell dysfunction.

47 esult in impaired glucose tolerance and beta-cell dysfunction.

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

49 of lung diseases characterized by epithelial cell dysfunction.

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

51 echanism of HHcy induced retinal endothelial cell dysfunction.

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

53 ion induces a sustained vascular endothelial cell dysfunction.

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

55 conducive to tumor progression and further T cell dysfunction.

56 istance, hyperglycemia, and progressive beta cell dysfunction.

57 ector functions, and variable natural killer cell dysfunctions.

58 lamic-pituitary axis disorders and male germ cell dysfunction, 62.0% [95% CI, 59.5%-64.6%]), cardiac

59 Adult beta-cell dysfunction, a hallmark of type 2 diabetes, can be

60 f unknown origin characterized by epithelial cell dysfunctions, accumulation of fibroblasts and myofi

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

62 T-cell dysfunction after PI seems to increase the risk of

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

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

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

66 Islet beta-cell dysfunction and aggressive macrophage activity are

67 n corrects existing diabetes-induced CD34(+) cell dysfunction and also confers protection from develo

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

69 -Phb2(-/-) mice was contributed by both beta-cell dysfunction and apoptosis, temporarily compensated

70 een implicated in hyperglycemia-induced beta-cell dysfunction and apoptosis.

71 proinsulin intermediates are markers of beta-cell dysfunction and are strongly associated with develo

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

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

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

75 Pancreatic beta-cell dysfunction and death are central in the pathogenes

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

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

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

79 PDMS-CaO(2) disk eliminated hypoxia-induced cell dysfunction and death for both cell types, resultin

80 r understanding of the pathways that lead to cell dysfunction and death in Parkinson's disease and Hu

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

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

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

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

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

86 d novel mechanisms of palmitate-induced beta-cell dysfunction and death.

87 antibody action, thus preventing myocardial cell dysfunction and death.

88 increasingly believed to be responsible for cell dysfunction and death.

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

90 of Bmal1, a core clock gene, results in beta-cell dysfunction and diabetes.

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

92 2 diabetes, may therefore contribute to beta-cell dysfunction and disease progression.

93 r maintain DNA methylation patterns leads to cell dysfunction and diseases such as cancer.

94 remains secondary to neuronal and epithelial cell dysfunction and does not irreversibly contribute to

95 spectrin cause ataxia, initially by Purkinje cell dysfunction and exacerbated by subsequent cell deat

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

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

98 1beta action by IL-1betaAb counteracted beta-cell dysfunction and glucose intolerance, supporting the

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

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

101 Beta-cell dysfunction and impaired insulin production are hal

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

103 T-cell dysfunction and increased infection were reversed b

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

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

106 stablished type 2 diabetes display both beta-cell dysfunction and insulin resistance.

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

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

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

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

111 es in a process that is associated with beta-cell dysfunction and loss of beta-cell mass.

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

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

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

115 2 diabetes mellitus (T2DM), the role of beta-cell dysfunction and peripheral insulin resistance (IR)

116 he toxic potential of hIAPP and enhance beta cell dysfunction and progression of T2DM.

117 antitumor activity while reducing systemic T cell dysfunction and promoting memory formation.

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

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

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

121 key mediator of apoptotic signaling and beta cell dysfunction and suggest that it may serve as target

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

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

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

125 pe 2 diabetes (T2D) is characterized by beta-cell dysfunction and the subsequent depletion of insulin

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

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

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

129 a heterogeneous disorder characterized by B-cell dysfunction and, in a subgroup, by expansion of CD2

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

131 e useful targets for controlling endothelial cells dysfunction and consequently atherosclerosis forma

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

133 ty, unprovoked ketoacidosis, reversible beta-cell dysfunction, and near-normoglycemic remission.

134 severity of tissue insulin resistance, beta-cell dysfunction, and oral fat intolerance (characterize

135 ption of pancreatic islet architecture, beta-cell dysfunction, and surprisingly, hypoglycemia.

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

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

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

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

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

141 Plasma markers of B-cell dysfunction are frequent after transplantation and

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

143 cause and the underlying mechanisms of alpha cell dysfunction are unknown.

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

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

146 h these mutations is caused by cochlear hair cell dysfunction, as indicated by conspicuous elongation

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

148 ecipients has suggested that pancreatic beta-cell dysfunction, as opposed to insulin resistance, may

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

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

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

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

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

154 pe 2 diabetes (T2D) pathophysiology and beta-cell dysfunction but have contributed little to the unde

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

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

157 believed to be pivotal in the development of cell dysfunction, but the mechanism of their formation i

158 Type 1 diabetes is preceded by islet beta-cell dysfunction, but the mechanisms leading to beta-cel

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

160 transgenic mouse models show that supporting cell dysfunction can cause SGN degeneration in the absen

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

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

163 ostprandial lipemia induces pancreatic alpha cell dysfunction characteristic of type 2 diabetes and,

164 A key feature of SLE is T cell dysfunction characterized by hyperresponsive antige

165 diabetes is associated with pancreatic alpha cell dysfunction, characterized by elevated fasting plas

166 oke (CS) that are associated with epithelial cell dysfunction, cilia shortening, and mucociliary clea

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

168 to whole-body glucose homeostasis, and beta-cell dysfunction contributes significantly to diabetes m

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

170 results establish that adult stem/progenitor cell dysfunction contributes to ageing-related degenerat

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

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

173 nd, therefore, propose that pancreatic alpha cell dysfunction could be viewed, at least partly, as a

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

175 nal traits shared in different settings of T cell dysfunction, distinctions between such dysfunctiona

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

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

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

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

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

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

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

183 rived suppressor cell (MDSC) expansion and T-cell dysfunction during human immunodeficiency virus typ

184 (IL-10) is an important factor involved in T-cell dysfunction during persistent viral infection.

185 important contributor to the degree of CD8 T cell dysfunction during viral persistence.

186 s arising from immune cells cause islet beta cell dysfunction even before overt hyperglycemia.

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

188 The relevance of B-cell dysfunction for progression to AIDS among human imm

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

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

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

192 2 diabetes (T2D) and its involvement in beta cell dysfunction has further highlighted the significanc

193 e relationship between PD-1 expression and T-cell dysfunction has not been delineated.

194 function, but the mechanisms leading to beta-cell dysfunction have not been rigorously studied.

195 NK cell dysfunctions have been reported in various hematolo

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

197 er risk of DM preceded predominantly by beta-cell dysfunction (HR = 0.33, 95% CI: 0.14, 0.80; and HR

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

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

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

201 ive stress, a condition associated with beta cell dysfunction in both type 1 diabetes (T1DM) and T2DM

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

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

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

205 In conclusion, despite evidence for global T-cell dysfunction in CLL, we show here that CLL-derived C

206 ted PD-1(+) T cells contribute to effector T-cell dysfunction in COPD.

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

208 beta-Cell dysfunction in diabetes results from abnormalities

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

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

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

212 Despite extensive evidence of B cell dysfunction in HIV disease, little is known about t

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

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

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

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

217 T cell dysfunction in solid tumors results from multiple m

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

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

220 ) stress has been suggested to underlie beta-cell dysfunction in T2D, its role in alpha-cell biology

221 ify EP3 as a new therapeutic target for beta-cell dysfunction in T2D.

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

223 Interestingly, phenotypic Sertoli cell dysfunction in the Arid4a(-/-)Arid4b(+/-) mice, inc

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

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

226 te recent clinical evidence implicating beta-cell dysfunction in the pathophysiology of new-onset dia

227 T cell dysfunction in the presence of ongoing antigen expo

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

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

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

231 gnaling could be a mechanism underlying beta cell dysfunction in type 2 diabetes.

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

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

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

235 can either result in functional memory or T cell dysfunction, including exhaustion, tolerance, anerg

236 ucial to develop targeted therapies for GC B cell dysfunctions, including lymphomas.

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

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

239 ased PTH is an independent predictor of beta-cell dysfunction, insulin resistance, and glycemia, high

240 fatty acids are known to associate with beta-cell dysfunction, insulin resistance, and increased inci

241 Pancreatic beta-cell dysfunction is a common feature of type 2 diabetes.

242 In particular, age-related T cell dysfunction is a major contributor to 'immune-senes

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

244 In most patients, beta cell dysfunction is associated with the presence of extr

245 Pancreatic beta cell dysfunction is pathognomonic of type 2 diabetes mel

246 Endothelial cell dysfunction is pivotal to the pathophysiology, but

247 T cell dysfunction is well documented during chronic viral

248 Insulin resistance (IR) and pancreatic beta-cell dysfunction lead to type 2 diabetes mellitus (DM).

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 Vascular endothelial cell dysfunction mediated by antiphospholipid antibodies

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

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

254 of patients with CVID, suggesting that CD4 T cell dysfunction might be caused by bacterial translocat

255 that cause local molecular damage leading to cell dysfunction, mutation, and cell death.

256 defined whether exhaustion contributes to T-cell dysfunction observed in chronic lymphocytic leukemi

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

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

259 Since beta cell dysfunction occurs during diabetes development, it

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

261 that was preceded predominantly by IR, beta-cell dysfunction, or both among 4,384 older adults (mean

262 er DM was preceded predominantly by IR, beta-cell dysfunction, or both.

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

264 These data show that beta-cell dysfunction persists after RYGBP, even in patients

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

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

267 iciency characteristic of both humoral and T cell dysfunction regularly found in human CVID.

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

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

270 B cell dysfunction should be considered in designing immun

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

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

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

274 cible ablation of the TCR resulted in T(reg) cell dysfunction that could not be attributed to impaire

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

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

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

278 dose administered, some mice develop Paneth cell dysfunction that resembles the intestinal phenotype

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

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

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

282 dition to revealing a link between EMT and T-cell dysfunction, these findings also show that ZEB1 pro

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

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

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

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

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

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

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

290 poor suppressive capacity indicating that T cell dysfunction was a global CD4(+) manifestation.

291 T cell dysfunction was antigen specific and did not depend

292 The TGRL-induced alpha cell dysfunction was due to reduced gamma-aminobutyric a

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

294 e development of insulin resistance and beta-cell dysfunction, whereas higher circulating levels of I

295 Loss of glucose tolerance was driven by beta-cell dysfunction, which correlated with abdominal fatnes

296 eta levels and consequent hematopoietic stem cell dysfunction, which is corrected by loss of Bak and

297 ding inflammatory gene expression and goblet cell dysfunction, which were associated with excess inte

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

299 beta cell dysfunction with subsequent apoptosis is considered

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