ライフサイエンスコーパス: anergy

1 ical role of functional unresponsiveness or 'anergy'.

2 d viability, and manifest characteristics of anergy.

3 discrimination between T cell activation and anergy.

4 proach predicated on the induction of B cell anergy.

5 e periphery, where they would be silenced by anergy.

6 and remained susceptible to anti-CD3-induced anergy.

7 rate to the liver where they induce NKT cell anergy.

8 her TCR stimulation is productive or induces anergy.

9 signals 1 and 2 by the HPCs mediated T-cell anergy.

10 -like nanoparticles (IDENs) induced NKT cell anergy.

11 in a state of functional impairment, termed anergy.

12 ion and is essential for induction of T cell anergy.

13 nment is important for induction of NKT cell anergy.

14 tions of suppression, TCR hyposignaling, and anergy.

15 to proliferate, confirming a state of T cell anergy.

16 ion results in a hyporesponsive state termed anergy.

17 cells, abortive T-cell activation and T-cell anergy.

18 anation of IL-2-mediated reversion of T-cell anergy.

19 of Ab production and promote loss of B cell anergy.

20 rous sclerosis (TSC)1 is critical for T-cell anergy.

21 breach of tolerance reflects loss of B cell anergy.

22 T cell responses and the induction of T cell anergy.

23 l, the autoreactive B cells are tolerized by anergy.

24 ation and reduced IL-2 secretion, suggesting anergy.

25 mechanisms, modulate B cell development and anergy.

26 ll trafficking, and T cell activation versus anergy.

27 ses, and may inhibit the induction of T-cell anergy.

28 ce are receptor editing, clonal deletion and anergy.

29 was unable to reverse established iNKT cell anergy.

30 ival was associated with alloreactive T cell anergy.

31 nsion of tumor-specific CTL without inducing anergy.

32 ptor and failure of IL-2 to break CD8 T cell anergy.

33 recessive tolerance mediated by deletion and anergy.

34 bortive attempt at activation and subsequent anergy.

35 tablishment of alphaGalCer-induced iNKT cell anergy.

36 (PI3K) lipid product PI(3,4,5)P(3) in B cell anergy.

37 zed that Cbl-b(-/-) T cells are resistant to anergy.

38 phosphatase SHIP-1 are required to maintain anergy.

39 d sufficient for the induction of T cell (T) anergy.

40 effector cytokines and prevention of T cell anergy.

41 d in subsequent immunological compromise and anergy.

42 -1-deficient mice failed to induce iNKT cell anergy.

43 T cell activation resulted in CD4(+) T cell anergy.

44 iphery in a state of unresponsiveness called anergy.

45 1-targeted therapies reverse TCD8 exhaustion/anergy.

46 cing T regulatory cells (T(REG)s) or causing anergy.

47 subsequently present it to induce CD4 T-cell anergy.

48 atients with zoster bear typical features of anergy.

49 and cbl-b in NKT cells, leading to NKT cell anergy.

50 uisition of effector functions or a state of anergy.

51 ties of this mechanism to those described in anergy.

52 signaling, plays a crucial role in iNKT cell anergy.

53 erentiation capacity may be a consequence of anergy.

54 induces a hyporeactive state that resembles anergy.

55 We have shown that B cell anergy, a major mechanism of B cell tolerance, is broken

56 eral tolerance mechanism is the induction of anergy, a refractory state in which proliferation and IL

57 e for the first time that HPCs induce T-cell anergy, a unique characteristic of iPSC-derived cells th

58 T-helper signals reversed the state of anergy, allowing BND cells to fully respond to antigenic

59 nder conditions that lead to the reversal of anergy, also induces Ndrg1 phosphorylation and degradati

60 ) regulatory T (Treg) cells and induction of anergy, an acquired state of T cell functional unrespons

61 The role of anergy, an acquired state of T cell functional unrespons

62 e molecules in regulating the choice between anergy and activation, a decision faced by all T cells u

63 pathogenesis is characterized by peripheral anergy and an exaggerated, pulmonary CD4(+) Th1 response

64 utoantibody transgenic studies indicate that anergy and apoptosis are involved, some studies claim th

65 lls have overall transcriptional features of anergy and apoptosis instead of neoplastic transformatio

66 umor-draining lymph nodes by inducing T-cell anergy and apoptosis through depletion of tryptophan and

67 uces signaling events in T cells, leading to anergy and apoptosis; however, active immunomodulation b

68 an VL, we examined molecules associated with anergy and cytotoxic T lymphocytes (CTL) in peripheral b

69 lopment of CHS by a mechanism involving both anergy and deletion of allergen-specific CD8(+) T cells

70 oaded, rescue CD8(+) T cells from peripheral anergy and deletion while stimulating islet-reactive CD4

71 l-b and Itch ligase activity regulate T-cell anergy and development of Foxp3+ regulatory T cells (Tre

72 accination with combination therapy reversed anergy and enhanced the expansion and function of CD8 T

73 tes immune tolerance through effector T-cell anergy and enhanced Treg function.

74 Our data show that NFAT promotes T cell anergy and exhaustion by binding at sites that do not re

75 l for untangling the molecular mechanisms of anergy and exhaustion in human B cells.

76 quired for antigen-specific T cell deletion, anergy and expression of regulatory markers.

77 rg1 contributes to the maintenance of clonal anergy and inhibition of T-cell-mediated inflammation.

78 E-mediated anaphylaxis by inducing mast cell anergy and later removing all mast cell IgE.

79 ve an indispensable role for GRAIL in T cell anergy and oral tolerance-a promising, antigen-specific

80 or knock-in mice Env(+)B cell clones develop anergy and partial deletion at the transitional to matur

81 n via the combined effects of cell-intrinsic anergy and regulatory T cell induction.

82 nhibit T-cell responses through induction of anergy and regulatory T cells in various model systems,

83 The roles of anergy and the indoleamine 2,3 dioxygenase (IDO)-tryptop

84 re the relationship between the induction of anergy and the induction of regulatory T cells as well a

85 SCs but also prevented tumor-specific T-cell anergy and Treg development.

86 gic autoreactive BND cells escape functional anergy and whether this process is altered in patients w

87 ally expanded peripheral B cells is prone to anergy and/or apoptosis.

88 hese mechanisms include T cell inactivation (anergy) and deletion.

89 l debris can drive clonal T-cell deletion or anergy, and antigens chemically coupled ex vivo to apopt

90 ment, predominantly by modulating apoptosis, anergy, and cell-cycle progression.

91 rance mechanisms, including clonal deletion, anergy, and clonal ignorance.

92 e of mechanisms, including clonal depletion, anergy, and immunoregulation, which act in a synergistic

93 ive selection mechanisms including deletion, anergy, and receptor editing were relatively unperturbed

94 anism in addition to clonal deletion, clonal anergy, and receptor editing.

95 L1 inhibits T and B cell activation, induces anergy, and reduces cytotoxicity in CD8(+) T cells.

96 ore, the relative contributions of deletion, anergy, and regulation have not been measured in a model

97 -cell hyporesponsiveness as a form of clonal anergy, and they supported an important role for CD4+ T-

98 olecular mechanisms of T cell activation and anergy, and we suggest that activators of Sirt1 may be u

99 nisms including receptor editing, functional anergy, and/or deletion.

100 deletion is circumvented, kappa editing and anergy are additional safeguards preventing 2F5 V(H)/V(L

101 Although T cell deletion and anergy are likely components of tolerogenic mechanisms i

102 CD161+ Treg display anergy, are suppressive in cocultures with conventional

103 Furthermore, we identify a loss of B cell anergy as a likely mechanism to explain the production o

104 or necrosis but did involve the induction of anergy as confirmed by the upregulation of early growth

105 absence of SHIP-1 in B cells led to loss of anergy as indicated by restoration of BCR signaling, los

106 was inversely correlated with the extent of anergy as measured by the ability to mobilize intracellu

107 ) immature B cells show similar hallmarks of anergy as those observed in mature splenic B cells.

108 hypothesized that such failure may be due to anergy, as CLL cells exhibit variable levels of nonrespo

109 lls generated from the original donor (i.e., anergy assay).

110 L-7/Akt/mTOR signaling cascade downregulates anergy-associated genes and upregulates activation- and

111 scription factor NFAT mediates expression of anergy-associated genes in the context of cancer.

112 ditions, the expression of a specific set of anergy-associated genes is activated.

113 cytokine production, elevated expression of anergy-associated genes, and diminished diabetogenicity.

114 nking, thus displaying a signature of B cell anergy at both biochemical and functional levels.

115 as neither required for Treg suppression nor anergy because costimulatory blockade by the external do

116 lly autoreactive and tolerized by functional anergy (BND cells).

117 W)F1 mouse lupus B cells by promoting B cell anergy, both in vitro and in vivo.

118 OVA-loaded exosomes did not induce iNKT cell anergy but were more potent than soluble alphaGC + OVA i

119 on of alpha-GalCer causes long-term NKT cell anergy, but the molecular mechanism is unclear.

120 treatment prevented the induction iNKT cell anergy, but was unable to reverse established iNKT cell

121 Acute breach of anergy by compromise of either of these pathways leads t

122 ata indicate that TSC1 is crucial for T-cell anergy by inhibiting mTORC1 signaling through both ICOS-

123 Induction of CD4(+) T cell anergy by LAM may represent one mechanism by which M. tu

124 chia coli; vi) MAIT cell hyperactivation and anergy co-utilize a signaling pathway that is governed b

125 s suggests the hypothesis that effector cell anergy could contribute to clinical desensitization.

126 kine responses to HPV proteins and reversing anergy could improve clinical outcomes for RRP patients.

127 face markers for differentiation (CD127) and anergy (cytotoxic T lymphocyte antigen 4 [CTLA-4] and pr

128 ct directly with antidonor T cells, inducing anergy, deletion, and/or regulation.

129 hat occurred during the initial induction of anergy did, however, allow the anergic CD4 T cells to ex

130 nfection or injury may, by disrupting B-cell anergy, dispose individuals toward autoimmunity, the pre

131 igens, could interact with the BCR to induce anergy early during B cell development.

132 This patient showed cutaneous anergy, even though he had normal numbers of peripheral

133 PD-L1 with PD-1 on donor CD8+ T cells cause anergy, exhaustion, and apoptosis, thereby preventing GV

134 ent CD8+ T cell expansion without increasing anergy, exhaustion, or apoptosis, resulting in strong GV

135 We suggest CD8 T cells are driven to anergy/exhaustion in human VL, which affect their abilit

136 ire, but that functional unresponsiveness or anergy exists in the mature B-cell repertoire along a co

137 Here we identify Ndrg1 as an anergy factor induced by Egr2.

138 these B cells are vulnerable to reversal of anergy following combined BCR/TLR engagement that promot

139 nct mechanisms, antigen addiction leading to anergy for naive T cells and ignorance for memory T cell

140 endotoxemia provide a rational basis for the anergy found in severe malnutrition.

141 es induced expression of DGK-alpha and other anergy genes and restores Ras/MAPK signaling, IL-2 produ

142 Basophil anergy has been characterized in vitro as a pathway-spec

143 er, the transcriptional regulation of T cell anergy has been poorly understood.

144 Several forms of anergy have been described and the past few years have b

145 ch as receptor editing, clonal deletion, and anergy, have been established in mice.

146 ucleotidase-adenosine system mediates T cell anergy in a human tumor.

147 nstrate that LAM upregulates GRAIL to induce anergy in Ag-reactive CD4(+) T cells.

148 melanoma, we found that cancer cells induced anergy in antigen-specific CD4+ T-cell populations, resu

149 fects of MDSCs might be mediated by inducing anergy in autoreactive T cells and the development of CD

150 on of CD4(+) T cells due to the induction of anergy in CHIKV-specific CD4(+) effector T cells.

151 pathogenic CD4+ T cells through induction of anergy in CHIKV-specific CD4+ Teff cells.

152 In conclusion, we demonstrate BCR anergy in CLL subset #4 and implicate TLR signaling and

153 supported an important role for CD4+ T-cell anergy in driving immune escape.

154 ls, we investigated the role of TLR7-induced anergy in HIV-1 infection.

155 Gene related to anergy in lymphocytes (GRAIL) is critical for the impair

156 that the E3 ubiquitin ligase gene related to anergy in lymphocytes (GRAIL) is expressed in quiescent

157 related with upregulation of gene related to anergy in lymphocytes (GRAIL) protein in CD4(+) T cells.

158 Gene related to anergy in lymphocytes (GRAIL, encoded by Rnf128) is an E

159 sly demonstrated that GRAIL (gene related to anergy in lymphocytes), a transmembrane RING finger ubiq

160 vation in non-mAAQ mice, and PD-L1-dependent anergy in mAAQ(+) hosts.

161 Thus, similar to mouse models, features of anergy in MC B cells rapidly revert after disengagement

162 tion and plays a major role in clonal T cell anergy in mice.

163 mTOR inhibitors induce anergy in naive T cells, promote the expansion of regula

164 Regulation and induction of anergy in NKT cells of the liver can inhibit autoimmune

165 Thus, chronic BCR signals maintain anergy in part via ITAM monophosphorylation-directed act

166 ll activation and proliferation, and promote anergy in recall response to Ag by CD4(+)CD44(+) T cells

167 iver where alpha-GalCer and PGE2 induced NKT anergy in response to subsequent alpha-GalCer stimulatio

168 eutralize HIV-1, establishing a key role for anergy in suppressing residual 2F5- or 4E10-expressing B

169 d macrophages induce severe unresponsiveness/anergy in T cells.

170 e that has recently been described to induce anergy in T cells.

171 c pathways during T cell activation leads to anergy in Th1-differentiated cells.

172 two subsets, as well as explore the role of anergy in the generation of peripheral Treg cells.

173 NFAT1 deficiency blunted the induction of anergy in tumor antigen-specific CD4+ T cells, enhancing

174 vides insights into the phenomenon of T-cell anergy in vivo and is distinct from the better understoo

175 proximal TCR signaling can result in T cell anergy, in which T cells are inactivated following an Ag

176 regulation of Sirt1 expression led to T cell anergy, in which the activity of the transcription facto

177 e region (IGHV) displays different states of anergy, indicated by reduced surface immunoglobulin M (s

178 enous interleukin (IL)-2 reversed the T cell anergy induced by activated HSC.

179 reported and is likely to reflect a state of anergy induced by chronic autoantigen stimulation.

180 These cells display both the features of anergy induced by continual engagement of the B-cell rec

181 GTP loading and may be a specific feature of anergy induced by DNA Ags.

182 ts as a barrier to autoimmunity by promoting anergy, inducing regulatory T cells, and inhibiting effe

183 sponsible for the activation of at least two anergy-inducing genes, Grail and Caspase3.

184 rease in Ca(2+) levels induced expression of anergy-inducing genes, such as Cbl-b, Egr2, and p27, thr

185 ticular importance in broadening our view of anergy-inducing signals.

186 orrectly discriminate between activating and anergy-inducing stimuli and produce IL-2 in the absence

187 indings also extend the role of GRAIL beyond anergy induction and maintenance, suggesting that endoge

188 ore explored the relationship between clonal anergy induction and the avoidance of autoimmune arthrit

189 cells, which suggest a mechanism to overcome anergy induction by the regulation of intracellular Ca(2

190 Thus, our data suggest that not only is anergy induction important in preventing autoimmunity bu

191 y receptor editing in the bone marrow and by anergy induction in the periphery.

192 ted activation of type II NKT cells leads to anergy induction in type I NKT cells and affords protect

193 models, we found that Egr2 is necessary for anergy induction in vivo.

194 cient CD4 T cells was sufficient to override anergy induction in WT T cells and to restore inducible

195 ulation is a critical parameter that confers anergy induction over effector differentiation, it has b

196 ver, the molecular mechanisms leading to NKT anergy induction remain unclear.

197 express soluble HEL, lack of Itpkb converts anergy induction to deletion.

198 Ag plays an important role in anergy induction where high supraoptimal doses lead to t

199 Thymocyte deletion, anergy induction, and agonist selection are all forms of

200 cterial Hsp65 leads to suppression of IL-17, anergy induction, and enhanced production of anti-mycoba

201 Cbl-b E3 ligase activity is critical for the anergy induction, as revealed by the similarity between

202 gest that NOD mice promote tolerance through anergy induction, but a small proportion of autoreactive

203 Cbl-b, previously shown to be essential in anergy induction, was found in both the central and the

204 usly unrecognized function of IRF8 in B cell anergy induction.

205 hown to be a barrier to CD4(+) T cell clonal anergy induction.

206 production, and proliferation upon attempted anergy induction.

207 egions controlling B cell responsiveness and anergy induction.

208 red sensitivity of TSC1-deficient T cells to anergy induction.

209 by TGF-beta, IL-10, and dexamethasone and to anergy induction.

210 hanced T-cell expansion and prevented T-cell anergy induction.

211 rgic state and knockout of the gene prevents anergy induction.

212 ecessary to rescue autoreactive B cells from anergy induction.

213 how that increasing the TCR signaling favors anergy induction.

214 erance, such high CD45 expression transforms anergy into deletion.

215 Induction of T-cell clonal anergy involves serial activation of transcription facto

216 Anergy is a critical physiologic mechanism to sensor sel

217 T cell anergy is a key tolerance mechanism to mitigate unwanted

218 Anergy is a state of long-term hyporesponsiveness in T c

219 T-cell anergy is a state of T cells that is hyporesponsive to s

220 Clonal anergy is an enigmatic self-tolerance mechanism because

221 Moreover, anergy is associated with reduced differentiation capaci

222 Resistance of TSC1-deficient T cells to anergy is correlated with increased signaling through th

223 hormone, but it is not clear when and where anergy is induced.

224 -) CD4 T cells in an in vivo system in which anergy is normally induced by a constitutively expressed

225 bility has been supported in models in which anergy is normally induced in vitro, or in vivo followin

226 How T-cell anergy is regulated is still poorly understood.

227 These results indicate that B cell anergy is reinforced by the exclusion of both TLRs and t

228 absence of T-cell help causes cell death or anergy is supported by in vivo studies of B cells that a

229 d maintenance of natural killer T (NKT) cell anergy is unknown.

230 s induced during the induction of CD4 T cell anergy, is also expressed in resting CD4 T cells.

231 bserved are consistent with an unresponsive, anergy-like T cell phenotype of latently HIV-1 infected

232 An anergy-like, unresponsive state of the host cells of lat

233 nergic synapse may play an important role in anergy maintenance, induction, or both.

234 esults in resistance to alpha-GalCer-induced anergy, manifested by increased expansion of and cytokin

235 ere down-regulated ex vivo and expressed the anergy marker Grail.

236 Using superantigen- and tumor-induced anergy models, we found that Egr2 is necessary for anerg

237 exhibiting neither conventional features of anergy nor appreciable receptor editing.

238 p in the lipid tail could neither induce NKT anergy nor enhance MDSCs accumulation.

239 In CD4+ T cells, clonal anergy occurs when the T-cell receptor is activated in t

240 Specifically, a transient reversal in the anergy of alloreactive lymphocytes is seen in parallel w

241 occur as a consequence of either deletion or anergy of antigen-specific T cells; induction of antigen

242 To prevent autoimmunity, anergy of autoreactive B cells needs to be maintained, t

243 reactive CD8(+) T cells and MHC-II-dependent anergy of CD4(+) T cells.

244 B cells, we find no evidence of deletion or anergy of cells specific for antigen not bound to membra

245 lCer result in long-term unresponsiveness or anergy of iNKT cells, severely limiting its efficacy in

246 Moreover, anergy of the CD4+ cell population from 4x mice was slig

247 duced by Paneth cells, and downregulation or anergy of the innate immune receptors themselves.

248 atory signals resulted in clonal deletion or anergy of the T cell, respectively.

249 eceptors with high affinity for antigen with anergy of the undeleted lower affinity cells maintains t

250 the elimination or functional inactivation (anergy) of T cells that do come to recognize self-peptid

251 the dependence of tumor-induced CD4+ T-cell anergy on NFAT1, our findings open the possibility of ta

252 However, Treg suppression and anergy only required the external domain of CTLA-4, wher

253 l hyporesponsiveness can be caused by clonal anergy or adaptive tolerance, but the pathophysiological

254 e absence of costimulation, this can lead to anergy or apoptosis of cognate T cells, a property that

255 ssues are normally regulated by induction of anergy or apoptosis.

256 ponse to stimuli that normally induce B cell anergy or B cell clonal ignorance.

257 e include T cell-intrinsic pathways, such as anergy or deletion, or exogenous tolerance mediated by r

258 CR determines whether CD8(+) T cells undergo anergy or deletion.

259 scaped thymic negative selection, leading to anergy or deletion.

260 sm of T cell unresponsiveness different from anergy or exhaustion, driven by TGF-beta signaling on tu

261 s for the fate of B cells: clonal expansion, anergy, or apoptosis.

262 enter a state of diminished function termed anergy, or are ignorant to the presence of self-antigen.

263 ysfunction, including exhaustion, tolerance, anergy, or senescence.

264 hanisms, such as receptor editing and clonal anergy, preventing the activation of B cells expressing

265 , explaining the costimulation dependence of anergy prevention.

266 ils that is consistent with pathway-specific anergy previously described in vitro.

267 and exhibited transcriptomic exhaustion and anergy profiles by gene set enrichment analysis.

268 tial transcriptional regulator of the T cell anergy program.

269 The anergy-promoting molecular milieu and function induced b

270 evidence suggests that receptor editing and anergy, rather than deletion, account for much of B-cell

271 gulates the expression of the Foxp3 gene and anergy-related E3 ubiquitin ligase genes.

272 The mechanisms leading to iNKT cell anergy remain poorly understood.

273 f GRAIL in mediating these aspects of T cell anergy remains unclear.

274 B cell anergy represents an important mechanism of peripheral i

275 ls but does not mediate CD28 independence or anergy resistance.

276 nduction was preceded by an initial phase of anergy reversal consisting in the loss of ERK phosphoryl

277 nt bacterial- or sulfatide-induced iNKT cell anergy, suggesting additional mechanisms of iNKT cell to

278 unity in the absence of triggering iNKT-cell anergy, supporting their application in the design of a

279 ly, IL-2, a cytokine that can reverse T-cell anergy, suppresses sirt1 transcription by sequestering F

280 Using the key anergy target gene diacylglycerol kinase (DGK) alpha as

281 alphaGalCer-mediated induction of iNKT cell anergy that can be targeted for the development of immun

282 IDEN-associated PGE2 also induces NKT cell anergy through modification of the ability of dendritic

283 Basophil anergy thus seems to function as activation barrier to p

284 liver microenvironment that induced NKT cell anergy to alpha-GalCer restimulation.

285 levels of lipid induced regulatory T cells, anergy to cancer, and oral tolerance.

286 latory effects and simultaneously negate Th2 anergy to drive effector responses into a long-term func

287 ll proportion of autoreactive T cells escape anergy to provoke type 1 diabetes.

288 n breaking or bypassing immune tolerance and anergy to tumor/self antigens.

289 insights on the mechanisms of tumor-induced anergy/tolerance and may help explain why some immunothe

290 antigen-positive periphery with no signs of anergy, unresponsiveness, or prior activation.

291 uced expression of GRAIL, a marker of T cell anergy; upon restimulation, these T cells showed reduced

292 ure of NFAT-containing complexes that induce anergy versus those that are activated during a producti

293 Intriguingly, SAA reverses T(reg) anergy via its interaction with monocytes to activate di

294 NK cell anergy was accompanied by impaired early signal transduc

295 ic model, we further demonstrate that B cell anergy was breached in IRF8-deficient mice.

296 In this study, we found that anergy was selectively induced in fetal antigen-specific

297 Inactivation of basophils ('basophil anergy') was observed in about 10% of the cohort.

298 B cells do not exhibit classical features of anergy, we found that mature, naive, autoreactive HKI B

299 rected transgenic mice show increased B cell anergy when VprBP is inactivated in B cells.

300 ls, results in long-term unresponsiveness or anergy, which severely limits its clinical application.