ライフサイエンスコーパス: anergic

1 conv and CD8 T cells in the end product were anergic.

2 recognize HLA-A2-expressing HPCs but became anergic.

3 t their OVA-specific CD4(+)-T cells were not anergic.

4 present experiments, these cells also became anergic.

5 sting that these autoreactive B cells may be anergic.

6 ceptor editing or clonal deletion may become anergic.

7 n-specific receptors are deleted or rendered anergic.

8 ific T cells from iTreg treated animals were anergic.

9 ylate tyrosines, demonstrating that they are anergic.

10 lation of B cells that render memory T cells anergic.

11 e deleted, with the remaining cells rendered anergic.

12 anner to a Th1 response, while others become anergic.

13 ewly produced B cells are destined to become anergic.

14 are carried by 5% of naive B cells that are anergic.

15 en-presenting compartment in IRF8(K108E) are anergic.

16 s challenging, as these cells may be rare or anergic.

17 n BCR (125Tg) and promote T1D, despite being anergic.

18 oth experienced and naive CD4(+) T cells, 3) anergic 125Tg B cells are more efficient than naive B ce

19 proliferation could uncouple T cell anergy, anergic 2C cells were transferred into RAG(-/-) recipien

20 Here, we demonstrate that in anergic 3H9/Vkappa8 and Ars/A1 B cells the normal endocy

21 CD4(+) T cells became anergic after their second encounter with a high-affinit

22 le to distinguish and differentially isolate anergic and activated T cells in vivo.

23 in the absence of costimulation are rendered anergic and are hyporesponsive when presented with Ag in

24 thermore, CD8 T cells from healthy mice were anergic and could not be activated by exogenous IL-2.

25 In Bim+/+ mice these B cells are anergic and die rapidly.

26 e human PSA-induced Tr1 cells are profoundly anergic and exhibit nonspecific bystander suppression me

27 s could not make GPI-specific CD4(+) T cells anergic and failed to control arthritis.

28 compared with those of HC subjects, were not anergic and had high TH2 cytokine production upon peanut

29 Both CD25 subsets were anergic and had potent suppressive properties in vitro a

30 By comparing anergic and nonanergic immunoglobulin-transgenic mouse s

31 These recruited iNKT cells were anergic and prevented concanavalin A-induced (ConA-induc

32 echanism associated with the emergence of an anergic and regulatory CTLA-4(+)IL-2(low)Foxp3(-) T cell

33 We have compared anergic and regulatory T cells of the same Ag specificit

34 we have compared gene expression profiles of anergic and regulatory T cells.

35 We also showed fewer anergic and senescent CD8(+) T cells in COVID-19 individ

36 The FoxP3(+)CD8(+) T cells were anergic and suppressed dendritic cell priming of naive r

37 -derived regulatory T cells in that they are anergic and suppressive.

38 T regulatory cells (Treg) in vivo, which are anergic and suppressive.

39 lls isolated from protected animals were not anergic and were fully competent to proliferate and prod

40 ased solely on CD4 and CD127 expression were anergic and, although representing at least three times

41 atory T cells (Tregs) can render these cells anergic and, therefore, functionally indistinguishable.

42 sms by which FoxP3 regulates the phenotypic (anergic) and the functional (suppressive) characteristic

43 proliferation and Ab production of control, anergic, and autoimmune-prone B cells.

44 ral lymphoid tissues were Ag-experienced and anergic, and some developed into regulatory cells.

45 genic CD4+CD25- T cells rendered these cells anergic, and the beta-catenin-mediated induction of aner

46 T cells rendered anergic are refractory to further stimulation and are ch

47 , and the remaining splenic kappa cells were anergic, arrested at a semi-mature stage without undergo

48 R2 costimulation (Ars-CCG/C3dg complexes) of anergic Ars/A1 B cells led to Ca(2+) mobilization in vit

49 In this study we show that anergic as well as acutely Ag-stimulated immature B cell

50 BAFF can rescue anergic autoreactive B cells from death, but only when c

51 e diverse B-cell repertoire of mice contains anergic autoreactive B cells, and if so, whether antigen

52 t to identify the molecular mechanism of how anergic autoreactive BND cells escape functional anergy

53 Using this model, the potential of anergic, autoreactive B cells to present Ag and activate

54 ressive activity implicates the autoreactive anergic B cell as an enforcer of immunological tolerance

55 re used for presumptive identification of an anergic B cell cohort within a normal repertoire.

56 PKCbeta deficiency induced an anergic B cell phenotype and preferentially inhibited au

57 ity may be latent in the pretolerance and/or anergic B cell pools.

58 In contrast, whereas TLR9-intact anergic B cells accumulate near the T/B border, TLR9-def

59 Anergic B cells are characterized by impaired signaling

60 Anergic B cells are unresponsive to antigen and die prem

61 VID with CD21(low) B-cell expansion resemble anergic B cells based on high constitutive pERK expressi

62 ults suggest that the Ag unresponsiveness of anergic B cells can be overcome by cross-reactive (self-

63 tential in the Ars/A1 transgene model, where anergic B cells express a dual-reactive Ag receptor that

64 hat may represent new biomarkers to identify anergic B cells in humans.

65 ed at the transitional stage of development, anergic B cells in the IRF8-deficient background were ab

66 Although anergic B cells in the IRF8-proficient background were b

67 ls, indicating the pathological relevance of anergic B cells in type 1 diabetes.

68 In the absence of CD72, anergic B cells inappropriately proliferated and survive

69 Anergic B cells remained metabolically quiescent, with o

70 lularly, resembling the trafficking block in anergic B cells repeatedly stimulated by self-antigen.

71 In a Hy10 antibody transgenic model where anergic B cells respond to a biophysically defined lysoz

72 Our findings show that, although anergic B cells transiently acquire an activated phenoty

73 Normal and anergic B cells were isolated for analyses of B cell sig

74 Using adoptive transfer of anergic B cells with subsequent acute induction of gene

75 s to adopt many of the classical features of anergic B cells, although such cells still secreted Ab.

76 found to be constitutively phosphorylated in anergic B cells, and activation of this inhibitory circu

77 at IRF8 was expressed at a high level in the anergic B cells, and an elevated level of IRF8 promoted

78 ation, a large proportion CD21(low)CD38(low) anergic B cells, and decreased antigen receptor repertoi

79 Biochemical analyses indicated that in anergic B cells, CD72 dominantly down-regulated BCR sign

80 hether B cells from patients with CVID, like anergic B cells, have defects in extracellular signal-re

81 splayed as low levels of IgM and high IgD on anergic B cells, masking a varying proportion of autoant

82 CR, JNK, which is activated in naive but not anergic B cells, regulated entry into late endosomes.

83 nd regulated, the molecular adaptor Cbl-b in anergic B cells, suggesting that Cbl-b may play a role i

84 d decreasing the threshold for activation of anergic B cells, thereby promoting autoreactivity.

85 found reduced generation of PI(3,4,5)P(3) in anergic B cells, which was attributable to reduced phosp

86 ients derives from the abnormal expansion of anergic B cells.

87 ating surface activation markers on purified anergic B cells.

88 apoptotic protein, Bim, controls the fate of anergic B cells.

89 by promoting immunoglobulin D expression in anergic B cells.

90 like receptor (TLR) signaling can reactivate anergic B cells.

91 receptor (BCR) signaling resembling those of anergic B cells.

92 Autoreactive anergic B lymphocytes are considered to be dangerous bec

93 (-), short-lived, BCR signaling-unresponsive anergic B-2 cells.

94 ouse model utilizing hen egg lysozyme (HEL) "anergic" B cells was studied.

95 and surprisingly, the T cells do not become anergic but instead have a Th2 phenotype.

96 However, we found that stimulation of anergic, but not naive T cells induced nuclear transloca

97 esent with low frequency and may be rendered anergic by the tumors that express them, we expanded LMP

98 memory B-cell subset and to an "exhausted," anergic CD21(low) memory B-cell subset in HIV(+) patient

99 induction of anergy did, however, allow the anergic CD4 T cells to expand to greater numbers when th

100 Anergic CD4(+) T cells and Treg cells share a number of

101 nscriptional repressor that silences IL-2 in anergic CD4(+) T cells, also restricts autocrine IL-2 pr

102 c cell function to elicit the development of anergic CD4(+) T cells.

103 ve T cells and restore the responsiveness of anergic CD4(+) T cells.

104 reated mice exposed to alloantigen exhibited anergic CD4(+)CD25(-) effector cells and regulatory CD4(

105 R) 7/8 stimulation, compared with relatively anergic CD4(-) pDCs.

106 th surviving thymocytes differentiating into anergic CD4(-)CD8(-) double-negative thymocytes positive

107 biquitin ligase with increased expression in anergic CD4+ T cells.

108 activity (and subsequent T cell function) in anergic CD8(+) T cells.

109 esponding increase in antigen experienced or anergic cell phenotype.

110 type, whereas CD8-PBMC have features of both anergic cells and CTLs.

111 hat remove I/i binding, clonal redemption of anergic cells appears efficient during physiological hum

112 Such anergic cells are characterized by B-cell receptor (BCR)

113 Anergic cells are unresponsive to the self-Ag that induc

114 n transfer into a new host and immunization, anergic cells can induce a pathologic autoimmune reactio

115 Anergic cells do not produce these cytokines in response

116 nergic transgenic B cells, these physiologic anergic cells exhibited high basal intracellular free ca

117 Anergic cells express transcripts that are associated wi

118 However, we discovered that anergic cells failed to phosphorylate the NF-kappaB p65

119 Thus maintenance of the unresponsiveness of anergic cells is critical for prevention of autoimmunity

120 express a distinct molecular signature, but anergic cells largely lack such a profile.

121 nterestingly, the in vivo immune response of anergic cells occurs without the formation of germinal c

122 ing Foxp3(+) nTregs, the converted Tregs are anergic cells with decreased proliferation and activatio

123 These cells retain some characteristics of anergic cells, in that they have elevated basal BCR sign

124 resent cytokine secreting effector cells but anergic cells, some of which can secrete IL-10 and can t

125 a block in nuclear localization of NFAT1 in anergic cells.

126 urther define a gene expression signature of anergic CLL cells consisting of several NFAT2-dependent

127 insulin-binding B cells are absent from the anergic compartment of some first-degree relatives and a

128 Neuropilin-1 expression in anergic conventional CD4(+) T cells was associated with

129 ly distinct from that of their quiescent and anergic counterparts; however, a number of recent breakt

130 with normal cerebrospinal fluid, an atypical anergic course of herpes simplex virus encephalitis shou

131 In contrast, the gut mucosa presented an anergic cytokine profile in relation to ANXA1 expression

132 These "anergic" DCs failed to support T cell proliferation.

133 TLR activation, and break self-tolerance in anergic DNA-reactive B cells.

134 n dialysis led to the generation of a highly anergic donor-specific medicinal product containing an a

135 on (IFN-gamma) is epigenetically silenced in anergic effector TH1 cells.

136 he CD4 receptor on T-helper cells results in anergic effects on T-cell recruitment and consequently a

137 ations, sequential Env administration rescue anergic Env(+) (non-edited) precursor B cells.

138 se cells revealed that they are Ag specific, anergic, express FoxP3, CTLA-4, and glucocorticoid-induc

139 ve brought to light an increasing number of 'anergic factors' involved in the induction and the activ

140 Anergic features and chemokine unresponsiveness could be

141 ioned recipients were rendered unresponsive, anergic, Foxp3(+), or type II cytotoxic T phenotype.

142 cascades, whereas higher Ag doses induced an anergic functional state.

143 acellular calcium flux with activation of an anergic gene-expression program dependent on the transcr

144 e specific expansion of the transitional and anergic IgD(+)IgM(-)CD27(-) B cell subsets.

145 self-antigens, cell transfers revealed that anergic IgM(low) IgD+ B cells form twice as many GC prog

146 toxoid provides evidence for reactivation of anergic IgM(low) IgD+ IGHV4-34+ B cells and removal of c

147 ecretion by chronically antigen-experienced (anergic) immunoglobulin transgenic and nontransgenic B c

148 fferences in the formation or composition of anergic immunological synapses.

149 n (sIg), and many are minimally activated or anergic in response to B-cell receptor (BCR) crosslinkin

150 n kinase signaling in T cells that were made anergic in vitro or in vivo.

151 Rather than being selectively rendered anergic in vivo, circulating survivin-specific CTLs were

152 signaling defects in CD8(+) T cells rendered anergic in vivo.

153 cular lymphoma (FL) infiltrating T cells are anergic, in part due to suppression by regulatory T cell

154 trate that anergic T cells are metabolically anergic, in that upon full stimulation (signals 1 plus 2

155 This is characterized by the presence of anergic, interleukin (IL)-10-secreting CD4(+) T cells wi

156 or effective tolerance induction and elicits anergic, interleukin (IL)-10-secreting regulatory CD4(+)

157 However, anergic islet-specific CD4 T cells were resistant to PD-

158 characteristics of chronically activated or anergic-like B cells and identify the immunosuppressive

159 mune-responsive monocyte state and that this anergic-like state is crucial for the virus ability to e

160 e they act as immune modulators, inducing an anergic-like state of NKT cells.

161 l depletion; rather, they act by inducing an anergic-like state.

162 4 blockade inhibited the effects of Tregs on anergic lupus B cells.

163 subsequent fate of monocytes, giving rise to anergic macrophage-like cells in tissue and the release

164 te, might provide novel insights to overcome anergic mechanisms mediated by APCs.

165 We show that in antigen-primed anergic murine CD4(+) T cells the linker for activation

166 lin-binding B cells occur exclusively in the anergic naive IgD(+), IgM(-) B-cell (BND) compartment.

167 r cell function and with the accumulation of anergic NK cells.

168 TGFbeta-induced FOXP3+ T cells were neither anergic nor suppressive and produced high levels of effe

169 ells in the bovine system, these are neither anergic nor suppressive.

170 tetramer-binding CD4 T cells did not become anergic or differentiate into Foxp3(+) regulatory T cell

171 eplenish anti-tumor T cells that have become anergic or exhausted from ex vivo expansion or exposure

172 IL-7Ralpha expression, suggesting they were anergic or undergoing deletion.

173 ent for ex vivo expansion (e.g., they may be anergic), or use TCRs distinct from those of allergic in

174 In contrast to the anergic peripheral blood Tregs, lymphoid organ Tregs had

175 Tregs have an intrinsically anergic phenotype and do not produce IL-2 or proliferate

176 Loss of Helios in Tregs breaks their anergic phenotype and results in derepression of the Il2

177 ve Ag by B6 AM14 Vkappa8 B cells promotes an anergic phenotype as reflected by suboptimal responses t

178 regulatory cells and Foxp3(-)FR4(hi)CD73(hi) anergic phenotype CD4(+) T cells compared with Bim(-/-)

179 Acquisition of the anergic phenotype correlated with upregulation of gene r

180 c ablation of Nfat2 leads to the loss of the anergic phenotype culminating in a significantly comprom

181 entifies NFAT2 as a crucial regulator of the anergic phenotype in CLL.NFAT2 is a transcription factor

182 sures stable expression of a suppressive and anergic phenotype in the face of intense inflammatory re

183 f Grail in mice leads not only to loss of an anergic phenotype in various models but also to hyperact

184 that NFAT2 is an important regulator for the anergic phenotype of CLL.

185 er corroborated in vivo, as reflected by the anergic phenotype of most rescued B cells in 2F5 V(H) x

186 expression as a key mechanism underlying the anergic phenotype of self-reactive T cells.

187 NFAT2 activity by FOXP3 is important for the anergic phenotype of T(REG), as ectopic expression of NF

188 terised by an indolent disease course and an anergic phenotype of their leukaemia cells, which refers

189 dicate that massive death contributes to the anergic phenotype of Treg in vitro and suggest modulatio

190 It has been an enigma that Treg exhibit an anergic phenotype reflected by hypoproliferation in vitr

191 ogrammed cell death-1 (PD-1), and acquire an anergic phenotype that interferes with their cognate fun

192 express very high levels of FoxP3, maintain anergic phenotype, and are potent suppressors capable of

193 e activating receptor exhibited an immature, anergic phenotype, but retained the capacity to upregula

194 g-experienced cells in NOD mice displayed an anergic phenotype, but this population decreased with ag

195 cells from Itpkb(-/-) IgHEL mice possess an anergic phenotype, hypoproliferate in response to cognat

196 m PBMCs of patients on dialysis showed a low anergic phenotype, incompatible with their eventual clin

197 ripheral T lymphocytes show an activated and anergic phenotype, reduced viability, and a restricted r

198 at splenic CD8 cell predominantly display an anergic phenotype, whereas CD8-PBMC have features of bot

199 s to develop a Folate receptor 4(hi)CD73(hi) anergic phenotype.

200 the majority of rescued B cells retained an anergic phenotype.

201 roduction, followed by the acquisition of an anergic phenotype.

202 murine CD4(+) T cell types with a described anergic phenotype.

203 to self-Ag in the periphery, resulting in an anergic phenotype.

204 ST2, ceased to proliferate, and acquired an anergic phenotype.

205 regs, contributing to the maintenance of the anergic phenotype.

206 ults in the acquisition of a hyporesponsive (anergic) phenotype by these cells.

207 Despite their anergic phenotypes, B6 AM14 Vkappa8 B cells can respond

208 A naturally occurring subpopulation of anergic polyclonal CD4(+) T cells, enriched for self ant

209 iferative population in vivo, rather than an anergic population as they were initially portrayed.

210 esponsiveness, reinforcing the idea that the anergic program favors the survival of leukemic lymphocy

211 bolished in vitro and in vivo, whereas their anergic properties in vitro were maintained.

212 eriphery of protected mice but do not become anergic, raising the question of how long-term tolerance

213 3G11 characterizes a distinct population of anergic/regulatory T cells.

214 d calcium signaling and thereby abrogated an anergic response to BCR stimulation in CLL cells.

215 se data demonstrate that PTEN regulates the "anergic" response of Tregs to IL-2 in vitro and Treg hom

216 The anergic responses correlated with diminished expression

217 In this study, we demonstrate that CD4(+) anergic responses to polyclonal TCR stimulation are pres

218 ses reported previously, the cells displayed anergic responses to polyclonal TCR stimulation.

219 To determine whether these T cells were anergic, sequestered in the spleen, or physically delete

220 Ndrg1 is upregulated by anergic signalling and maintained at high levels in rest

221 Intriguingly, the anergic splenic T cells, although nonproliferative and u

222 Overexpression of Ndrg1 mimics the anergic state and knockout of the gene prevents anergy i

223 nvert into effector T cells and regain their anergic state and suppressive activity upon proliferatio

224 are maintained in a functionally silenced or anergic state by endogenous hormone, but it is not clear

225 es (pH 6-6.5) was sufficient to establish an anergic state in human and mouse tumor-specific CD8(+) T

226 class II to naive CD4 T cells, leading to an anergic state in the T cells.

227 2 as a critical component in controlling the anergic state in vitro.

228 , cAMP repression additionally abrogates the anergic state of human Treg, accompanied by nuclear tran

229 e efficacy was linked to the reversal of the anergic state of NK cells that specifically occurred in

230 The T cell anergic state persisted after the removal of LAM.

231 rate MHC class I-deficient tumors acquire an anergic state that can be reversed by particular combina

232 This anergic state was reversed by exogenous IL-2 and IL-15.

233 The transition from effector to anergic state was substantially faster in ST2-deficient

234 iacylglycerol metabolism could overcome the "anergic state" and support the ability of Tregs to up-re

235 ored BCR functionality, likely breaching the anergic state, and this was accompanied by induction of

236 IFN-alpha did not affect the anergic state, cytokine production, Foxp3 expression, or

237 tral transcription factor that regulates the anergic state.

238 uitin ligases are important mediators of the anergic state.

239 al individuals in a functionally inactive or anergic state.

240 ximately 92 cluster in the regulation of the anergic state.

241 n is, however, frustrated by their scarcity, anergic status, and lack of defined specificity.

242 he present work, we further investigated the anergic subset of CLL (defined as the one with constitut

243 ted by restoration of BCR signaling, loss of anergic surface phenotype, and production of autoantibod

244 ll increases in total phosphotyrosine at the anergic synapse along with significant decreases in phos

245 This Cbl-b (and c-Cbl) accumulation at the anergic synapse may play an important role in anergy mai

246 al supramolecular activation clusters of the anergic synapse.

247 cific accumulation of c-Cbl and Cbl-b to the anergic synapses.

248 Manipulations that induced or mimicked an anergic T cell state promoted latent HIV-1 infection.

249 velly shown to characterize trauma patients' anergic T cells and correlate with predominance of inhib

250 onsistently, CD80 expression was detected on anergic T cells and further up-regulated when they were

251 A major difference between anergic T cells and T cells undergoing peripheral deleti

252 In this report we demonstrate that anergic T cells are metabolically anergic, in that upon

253 In this issue of Immunity, demonstrate that anergic T cells are selectively defective in LAT activat

254 GRAIL is thought to selectively function in anergic T cells but its mechanism of action and its role

255 in-specific cells did not become effector or anergic T cells but remained naive.

256 ration of the ability to identify and purify anergic T cells by a distinct cell surface marker in an

257 Only patients' anergic T cells had simultaneously increased levels of t

258 Anergic T cells have altered diacylglycerol metabolism,

259 To date, several subsets of anergic T cells have demonstrated altered interactions w

260 ne diseases, yet no surface marker unique to anergic T cells in these diseases has been identified.

261 :peptide, and ICAM-1 staining, we found that anergic T cells make mature immunological synapses with

262 e of B7-H1 and PD-1 interaction could render anergic T cells responsive to antigen.

263 The anergic T cells survived, but were not immunoregulatory.

264 Importantly, adoptive transfer of these anergic T cells upon autoimmune disease induction had a

265 tor T cells, whereas established tolerant or anergic T cells were not dependent on PD-1/PD-L1 signali

266 In anergic T cells, activated caspase 3 associated to the p

267 y regulate Ras activity, were upregulated in anergic T cells, and a DGK inhibitor restored interleuki

268 aspects of immunological synapses formed by anergic T cells, but it remains unclear whether there ar

269 Similarly, IL-2 treatment of anergic T cells, under conditions that lead to the rever

270 d that Sirt1 expression is highly induced in anergic T cells.

271 ide further insight into the cell biology of anergic T cells.

272 s to analyze the initial signaling events in anergic T cells.

273 hibitor restored interleukin 2 production in anergic T cells.

274 t membrane (DRM) fractions were defective in anergic T cells.

275 ell population that phenotypically resembles anergic T cells.

276 ing and maintained at high levels in resting anergic T cells.

277 tion threshold for T cells; 2) is induced in anergic T cells; and 3) protects against autoimmunity.

278 PD-L1 signaling also induced an anergic T-bet(-)IFN-gamma(-) phenotype in CD8(+) T cells

279 Patients' proliferation hyporesponsive (anergic) T cells had increased expression of novel inhib

280 ing Treg encounter with that of T cells made anergic, TGF-beta-treated, or IL-2-deprived; all possibl

281 encing of the expression of the Ifng gene in anergic TH1 cells.

282 CD4+ T cells to expand and shift toward an "anergic" Th2 T-cell phenotype largely absent in both pre

283 uggested a resemblance with B cells rendered anergic through chronic autoantigenic stimulation.

284 leted or rendered functionally unresponsive (anergic), thus preventing them from propagating host tis

285 us-derived Tregs were phenotypically normal, anergic to allostimulation, and suppressed proliferation

286 elf-reactive T cells, but these cells became anergic to antigen stimulation.

287 rization in which they become hyporesponsive/anergic to antigenic stimulation.

288 d type 1 diabetes in NOD mice, despite being anergic to B cell mitogens and T cell-dependent immuniza

289 xp3(+) regulatory T cells (Treg), which were anergic to direct CD3 stimulation and mediated T cell su

290 ere we found that intestinal phagocytes were anergic to ligands for Toll-like receptors (TLRs) or com

291 Like anergic transgenic B cells, these physiologic anergic ce

292 , as previously suggested, but also distinct anergic type 3 B cells, as well as IL-10-producing CD27(

293 ways that are consistent with the idea of an anergic, unresponsive T cell phenotype.

294 mice have an impaired ability to be rendered anergic upon Ag engagement.

295 Interestingly, anergic Vbeta8(+) T cells isolated from staphylococcal e

296 with supraphysiologic CD45 expression became anergic, whereas only mice harboring the E613R mutation

297 The resulting GFP(+) TCR75 cells were anergic, whereas the GFP(-) TCR75 cells proliferated upo

298 bl-b expression increased in self-Ag-induced anergic wild-type CD4 T cells, and Cbl-b(-/-) CD4 T cell

299 These tolerant T cells not only were anergic with profound defects in TcR signal transduction

300 e frequency in males versus females and were anergic with respect to peptide activation, although thi