ライフサイエンスコーパス: anergic

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

2 present experiments, these cells also became anergic.

3 sting that these autoreactive B cells may be anergic.

4 ceptor editing or clonal deletion may become anergic.

5 n-specific receptors are deleted or rendered anergic.

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

7 ific T cells from iTreg treated animals were anergic.

8 ylate tyrosines, demonstrating that they are anergic.

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

10 e deleted, with the remaining cells rendered anergic.

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

12 ewly produced B cells are destined to become anergic.

13 tosis, and the survivors became functionally anergic.

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

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

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

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

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

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

20 Unlike B cells in other models of tolerance, anergic 125Tg B cells are not arrested in development, a

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

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

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

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

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

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

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

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

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

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

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

32 By comparing anergic and nonanergic immunoglobulin-transgenic mouse s

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

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

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

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

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

38 perhaps due to this capability of acquiring anergic and suppressive properties.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

61 Anergic B cells are characterized by impaired signaling

62 Anergic B cells are unresponsive to antigen and die prem

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

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

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

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

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

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

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

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

71 Anergic B cells remained metabolically quiescent, with o

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

89 ating surface activation markers on purified anergic B cells.

90 apoptotic protein, Bim, controls the fate of 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 + effector T cells and CD4+ T cells rendered anergic by TCR ligation in the absence of CD28 costimula

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

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

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

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

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

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

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

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

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

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

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

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

110 xpectedly, the CD8+CD161+ cells contained an anergic CD8alpha+CD8betalow/-CD161high T cell subset tha

111 esponding increase in antigen experienced or anergic cell phenotype.

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

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

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

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

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

117 Anergic cells do not produce these cytokines in response

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

119 Anergic cells express transcripts that are associated wi

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

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

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

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

124 Many features of anergic cells were rapidly reversed after dissociation o

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

143 Anergic features and chemokine unresponsiveness could be

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

164 4 blockade inhibited the effects of Tregs on anergic lupus B cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

204 to self-Ag in the periphery, resulting in 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 A naturally occurring subpopulation of anergic polyclonal CD4(+) T cells, enriched for self ant

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

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

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

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

212 3G11 characterizes a distinct population of anergic/regulatory T cells.

213 ore, we provide evidence to indicate that an anergic response to B cell receptor stimulation may be r

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

215 The anergic responses correlated with diminished expression

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

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

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

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

220 Responsive Th2 lymph node T cells and anergic splenic lymphocytes were immortalized, and the s

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 hat is rescued by estrogen was present in an anergic state in mice treated with both estradiol and ta

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

228 2 as a critical component in controlling the anergic state in vitro.

229 ill be used to activate iNKT cells given the anergic state it has been shown here to induce?

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

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

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

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

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

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

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

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

238 tral transcription factor that regulates the anergic state.

239 uitin ligases are important mediators of the anergic state.

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

241 al individuals in a functionally inactive or anergic state.

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

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

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

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

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

247 al supramolecular activation clusters of the anergic synapse.

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

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

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

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

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

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

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

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

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

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

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

259 Anergic T cells have altered diacylglycerol metabolism,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

274 hibitor restored interleukin 2 production in anergic T cells.

275 t membrane (DRM) fractions were defective in 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 Patients' proliferation hyporesponsive (anergic) T cells had increased expression of novel inhib

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

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

281 comprised of Th2 cells in the lymph node and anergic Th1 lymphocytes in the spleen.

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