ライフサイエンスコーパス: memory cell

1 tal memory populations (central and effector memory cells).

2 electrodes confining the resistive switching memory cell.

3 an operate as an energy efficient multilevel memory cell.

4 in the tumor-bearing host, and persisted as memory cells.

5 stics of both early effectors and long-lived memory cells.

6 development of circulating and lung-resident memory cells.

7 ls and their differentiation into functional memory cells.

8 mpaired proliferation and reduced numbers of memory cells.

9 receptor 3 (CXCR3)(lo)CD43(lo) effector-like memory cells.

10 s magnetic nanomotors, actuators, sensors or memory cells.

11 ng were predominantly (mean 97.5%) CD45RO(+) memory cells.

12 to have multiplexed quantum memory with many memory cells.

13 the transcriptional program associated with memory cells.

14 nes, thereby accelerating the development of memory cells.

15 ate 'decisions' involved in the formation of memory cells.

16 esponding to a melanoma tumor than wild-type memory cells.

17 s population composed of both naive (TN) and memory cells.

18 D4(+) T cells as well as mature effector and memory cells.

19 pirical and more predictive design of future memory cells.

20 f memory precursor WP T cells into long-term memory cells.

21 eted of IL-2 that are differentiating toward memory cells.

22 rication of atomic-scale, robust planar Ag2S memory cells.

23 and functional characteristics of long-lived memory cells.

24 s some cells in the clonal population become memory cells.

25 T cell response and its differentiation into memory cells.

26 ential for survival of naive T cells but not memory cells.

27 T follicular helper (TFH) cells and non-TFH memory cells.

28 g at a defined effector checkpoint to become memory cells.

29 ell number and the development of long-lived memory cells.

30 ociation with reduced PD-1 expression on CD4 memory cells.

31 cing plasma cells, germinal center cells, or memory cells.

32 with these cross-reactive NP205-specific CD8 memory cells.

33 ts the activity of GVH-reactive primed T and memory cells.

34 not complete differentiation programs toward memory cells.

35 (TGF-beta) signaling but were true resident memory cells.

36 cells (MPECs), which ultimately develop into memory cells.

37 entary organic circuits, and two nonvolatile memory cells.

38 -specific T effector cells into long-lived T memory cells.

39 ignaling impairs the development of effector memory cells.

40 y T cells but also memory B cells and innate memory cells.

41 p B cells become long-lived plasma cells and memory cells.

42 hes Helios(+)FOXP3(+) from Helios(-)FOXP3(+) memory cells.

43 mming, which enhanced the generation of CD8+ memory cells.

44 d differential methylation between naive and memory cells.

45 de of the immune response, and in generating memory cells.

46 for the development of these unconventional memory cells.

47 nto Th17 cells, as well as expansion of Th17 memory cells.

48 erentiation of B cells into plasma cells and memory cells.

49 efects in expansion and differentiation into memory cells.

50 erentiation of activated CD8(+) T cells into memory cells.

51 n numbers similar to those of virus-specific memory cells.

52 ing contraction, generating a larger pool of memory cells.

53 ed effectors and a stable pool of long-lived memory cells.

54 ecursor cells or are needed later to sustain memory cells.

55 nature akin to that of established T central memory cells.

56 oting their differentiation to allo-specific memory cells.

57 en-non-specific BRM cells were maintained as memory cells.

58 that this reservoir resides primarily within memory cells.

59 photomagnetic molecules as future molecular memory cells.

60 arrier by unifying storage with computing in memory cells.

61 receptors and differentiated into long-lived memory cells.

62 (+) CD57(-)-resembling proliferation-capable memory cells.

63 fector checkpoint to most efficiently become memory cells.

64 ted that these cells were neither plasma nor memory cells.

65 f the gut homing receptor CCR9 on T-effector memory cells 30 days after transplant was increased in c

66 nal diversity makes therapeutic targeting of memory cells a challenging task in transplantation.

67 tate, the subset of cells that gives rise to memory cells acquired de novo DNA methylation programs a

68 ave been found to better persist as effector/memory cells after a peripheral challenge.

69 t CD8(+) T cells selectively form long-lived memory cells after infection because they are derived fr

70 s, and then contract to a long-lived pool of memory cells after pathogen clearance.

71 espite the induction of Th1-specific central memory cell and effector memory cell responses highlight

72 lating Tfr and Tfh cells share properties of memory cells and are distinct from effector Tfr and Tfh

73 sembling terminally differentiated senescent memory cells and CD127(+) CD57(-)-resembling proliferati

74 compartment revealed expansion of T effector memory cells and concomitant loss of a CD4(+) T cell pop

75 All subsets formed memory cells and expressed markers previously identified

76 tion to upregulate the fraction of T central memory cells and expression of CCR5, which enhances susc

77 T cells are enriched in CD8(+) and CD45RO(+) memory cells and in CCR7(-) cells.

78 ons, such as poor induction of immunological memory cells and inefficient T effector cells.

79 Additional markers for effector memory cells and inflammatory function were elevated in

80 ng of memory cells, focusing on diversity of memory cells and mechanisms involved in their induction

81 ore than one million resistive random-access memory cells and more than two million carbon-nanotube f

82 proteins studied were predominantly effector memory cells and produced both cytotoxic (CD107a express

83 tum memory with many individually accessible memory cells and programmable control of its addressing

84 entiation to enable generation of long-lived memory cells and protective immunity after viral infecti

85 al qubits can be stored into any neighboring memory cells and read out after a programmable time with

86 CD90.1+Foxp3-IL-10+ Tr1 cells arise from memory cells and rejoin the tissue-resident memory T-cel

87 ly early (1 d) after activation of naive and memory cells and that demethylation is the predominant c

88 Little is known about allergen-specific Th2 memory cells and their contribution to airway inflammati

89 ed," virus-specific B cells, i.e., activated memory cells and tissue-like memory B cells.

90 cells into CD138(+) plasma and IgD(-)CD27(+) memory cells and triggered immunoglobulin secretions.

91 ing how viral clearance might be mediated by memory cells and what functions should be induced by vac

92 -alpha- and IFN-gamma-producing Th1 effector memory cells, and IL-33-stimulated cells showed an equiv

93 roducing effector plasmablasts/plasma cells, memory cells, and immune regulatory B cells.

94 ent physical systems--well isolation for the memory cells, and strong interactions for the transmissi

95 een activation, which generates effector and memory cells, and suppression, which is mediated mainly

96 ved plasma cells, germinal center cells, and memory cells; and how each path impacts antibody diversi

97 Memory cells are a critical component of protective immu

98 The existing ferroelectric memory cells are based on the two-level storage capacity

99 vation of both naive and memory T cells, the memory cells are capable of producing lineage specific c

100 entral memory differentiation of RTE-derived memory cells are counterbalanced by their increased prol

101 Memory cells are heterogeneous, including not only memor

102 Immune memory cells are poised to rapidly expand and elaborate

103 peat infection, dengue virus-specific immune memory cells are reactivated and large amounts of antibo

104 sms behind this rapid recall response of the memory cells are still not completely understood.

105 Memory cells are the products of immune responses but al

106 Although memory cells are the progeny of naive T cells, it is unc

107 CD8(+) CD62L(-) KLRG1(+) CD107a(+) effector-memory cells, are the main producers of IL-33 in these H

108 t's noise, intrinsic and/or extrinsic to the memory cell array.

109 es thus identify IL-2-dependent resident Th2 memory cells as drivers of lung allergic responses.

110 , compared with Ge2Sb2Te5-based phase change memory cell at the same size.

111 for HIV-1 DNA was recorded in peripheral CD4 memory cells at 28 months.

112 lations are continuously supplemented by new memory cells at rates that are independent of environmen

113 n the rates of homeostatic proliferation and memory cell attrition.

114 s, as well as activated T-cell effectors and memory cells; B-cell follicles containing follicular den

115 Here, we report an oxide-free, floating-gate memory cell based on III-V semiconductor heterostructure

116 Here, we demonstrate phase change memory cell based on Ti0.4Sb2Te3 alloy, showing one orde

117 Resistive switches are non-volatile memory cells based on nano-ionic redox processes that of

118 Temporal GC analysis suggests B memory cells (Bmem) are generated early, while LLPCs are

119 (IFN-gamma) and can transition to long-lived memory cells but are not polyfunctional.

120 erentially into memory precursor and central memory cells, but also produce more cytokines.

121 ng the transition from naive to effector and memory cells, but mechanisms controlling this process ha

122 ed more extensively than did 4-1BB-generated memory cells, but these cells failed to persist.

123 he burst effector size enables generation of memory cells by CD8(+) T cells, regardless of CD4 help.

124 c studies have demonstrated that circulating memory cells can be further divided into effector memory

125 Alloreactive memory cells can mount rapid and robust responses to the

126 nt LDH inhibition enhanced the generation of memory cells capable of triggering robust antitumor resp

127 Allospecific CD154+T-cytotoxic memory cells (CD154+TcM) predict acute cellular rejectio

128 T effector/memory cells (CD4(+) CD25(lo) ) were increased at 6 h an

129 and found a strong antigen specific central memory cell (CMC) response with increased Th1 and Th17 c

130 ic circuits, such as reprogrammable volatile memory cells, complementary inverters and OR logic gates

131 Here we demonstrate an array of cryogenic memory cells consisting of a non-volatile three-terminal

132 +), T regulatory (Treg) effector and central memory cells, converted naive CD4(+) T cells into induce

133 of which 39 exhibited reduced methylation in memory cells coupled with increased gene expression upon

134 Importantly, the subsequent persistence of memory cells derived from this pool was also qualitative

135 nts a technological breakthrough towards new memory cell designs.

136 ance against respiratory viral infection and memory cell development.IMPORTANCE B cells play critical

137 On memory cell differentiation and in most EBV-associated B

138 rs regulate the balance between effector and memory cell differentiation during T cell activation.

139 ble factor regulator Vhl, accelerated CD8(+) memory cell differentiation during viral infection.

140 tantly, BCG vaccination induced effector and memory cell differentiation of gammadelta T cells in bot

141 Reduced memory T-cell survival and altered memory cell differentiation were associated with up-regu

142 in cell fate decisions such as effector and memory cell differentiation, and in regulatory T cell fu

143 ange of effects in B cells, including skewed memory cell differentiation, compromised B cell function

144 redefine the role of cellular metabolism in memory cell differentiation, showing that reliance on gl

145 s the phenotype and function of effector and memory cell differentiation.

146 environmental cues for clonal expansion and memory cell differentiation.

147 higher frequencies of CD8 Tem and T central memory cells displayed effector functions in response to

148 ly all microbe-specific naive cells produced memory cells during infection.

149 r potential to form circulating effector and memory cells during recall responses.

150 Thus, memory cells embody features of both naive and effector

151 Despite sustained glycolysis, CD8(+) memory cells emerged that upregulated key memory-associa

152 characterized by reduced numbers of effector memory cells, especially CD8(+) TEMRA cells (3.37 +/- 1.

153 RTE-derived and mature memory cells expanded equivalently during rechallenge, i

154 Nef- and Env-specific memory cells expanded poorly for all groups, and their e

155 Here we show that elementary-shape memory cells fabricated from a single-layer antiferromag

156 However, these reactivated memory cells failed to survive.

157 de by B cells, favoring the plasma cell over memory cell fate without significantly affecting clonal

158 ct tendencies to adopt terminal effector and memory cell fates.

159 ight recent advances in our understanding of memory cells, focusing on diversity of memory cells and

160 More CD8(+) T cells differentiate to memory cells following GFP-DDDHA infection than after in

161 vival and a reduced capacity to develop into memory cells following stimulation with cognate Ag plus

162 n in tandem with the induction of long-lived memory cells for effective recall immunity.

163 eam of IFNAR) are defective in expansion and memory cell formation after mouse cytomegalovirus (MCMV)

164 aling pathways are altered to promote CD8(+) memory cell formation and rapid responses to and protect

165 lation of programmed cell death-1 and absent memory cell formation, consistent with a dysfunctional p

166 T cells eliminates the observed increase in memory cell formation.

167 ated that Thpok cell-intrinsically protected memory cells from a dysfunctional, effector-like transcr

168 ional circuitry controlling the emergence of memory cells from early CD4(+) antigen-responders remain

169 expansion, only 18% of the tetramer-binding memory cells from healthy subjects versus 79% in CD pati

170 is likely to represent migration of effector memory cells from the skin to the LN.

171 (+) memory B cells, Th1, Th2, Th17, and Treg-memory cells from venous blood.

172 tion potential of the Ab-secreting cells and memory cells generated upon immunization.

173 about the effect of low-affinity priming on memory cell generation and function, which is particular

174 T cell proliferation, effector function, and memory cell generation in response to infection with lym

175 asing oligoclonality but also interfere with memory cell generation.

176 ation, analogous to T-cell effector cell and memory cell generation.

177 Batf3 (-/-) memory cells had an impaired ability to mount a robust r

178 s to adapt and differentiate into long-lived memory cells has added further complexity to this field.

179 (GO) based low cost flexible electronics and memory cell have recently attracted more attention for t

180 It is not known if memory cells have a higher synapse propensity (SP; i.e.,

181 Ara h 2-specific sequences from memory cells have rates of nonsilent mutations consisten

182 Moreover, in Th17 memory cells, IL-21 selectively inhibited T-bet upregula

183 mristors to replace the static random-access memory cell in conventional designs, but employ similar

184 ntum memory with 225 individually accessible memory cells in a macroscopic atomic ensemble.

185 nges in cytotoxic capacity in virus-specific memory cells in detail.

186 D patients, indicating that tetramer-binding memory cells in healthy control subjects may be cross-re

187 ificantly up-regulated in activated effector memory cells in humans, suggest that these analogues rep

188 e local epidermal skin, enhanced circulating memory cells in the blood, and showed protection from in

189 he challenges and opportunities in targeting memory cells in the induction of transplant tolerance.

190 data suggest that the low levels of effector memory cells in the LN may explain the low background of

191 s in the lymphoid organs and tissue-resident memory cells in the lung.

192 ted in persistent TH2/TH17 CD127(+) effector/memory cells in the lungs, spleen, and lymph nodes of ad

193 M-specific memory cells persisted as central memory cells in the lymphoid organs and tissue-resident

194 in-derived signals also affect recirculating memory cells in the skin remains unclear.

195 se polyomavirus-specific CD8 T cells, unlike memory cells in the spleen, progressively increase bindi

196 stently proliferated and differentiated into memory cells in vivo.

197 cific CD8(+) T cells, both Tem and T central memory cells, in lungs of animals subsequently challenge

198 iverse range of innate effector and adaptive memory cells, including follicular memory T cells and me

199 recruitment of blood-borne naive and central memory cells into lymph nodes.

200 t the number of insulin tetramer(+) effector memory cells is directly correlated with insulin antibod

201 Such a dichotomy between naive and memory cells is not observed within the human CD4 or mur

202 amental limit, vertical stacking of multiple memory cell layers, innovative device concepts, and nove

203 the naive pool strongly impact estimates of memory cell lifetimes and division rates.

204 have reported dysregulation of effector and memory cells, little is known about the effects on naive

205 CXCR4-deficient CD8(+) T cells have impaired memory cell maintenance due to defective homeostatic pro

206 infection but do not require this signal for memory cell maintenance or recall responses.

207 Individual magnetic memory cells measured at 4 K show reliable switching wit

208 ates that CD8alphabeta(+)NKG2D(+) T effector memory cells mediate alopecia areata in part through Jan

209 D8 T cell response to Listeria monocytogenes Memory cells mounted larger secondary responses and conf

210 Each memory cell needs to be individually addressable and ind

211 ed into a heterogeneous pool of effector and memory cells, neonatal CD8+ T cells preferentially gave

212 s; thus, infection detection rates depend on memory cell number and distribution.

213 Further, T cell clones of tetramer-sorted memory cells of healthy individuals showed lower gluten-

214 artificial memories can be inserted into the memory cells of the hippocampus in a way that is indisti

215 ted Ag for 3 d or less and generated few CD4 memory cells or long-lived Ab-producing B cells.

216 requency of HIV-1 DNA is typically higher in memory cells, particularly in the central memory (TCM) c

217 After allergen exposure, HDM-specific memory cells persisted as central memory cells in the ly

218 the virus, a small population of long-lived memory cells persists.

219 normally but failed to survive and seed the memory cell pool in both the lungs and spleen.

220 relative to their contribution to the CD4 T memory cell pool.

221 nded, functional, tissue-associated effector memory cell pools.

222 ector, central and terminally differentiated memory cell population and increased ICOS and BCL6 expre

223 to sensitively control immune tolerance and memory cell population size, but the molecular basis for

224 distinct from the precursors of circulating memory cell populations at the levels of gene expression

225 Different clonal memory cell populations had different B cell or macropha

226 Return of CD4 and CD8 T central and effector memory cell populations was rapid.

227 results outline a temporal model for loss of memory cell potential through selective epigenetic silen

228 aive cells from a polyclonal repertoire have memory cell potential.

229 l differentiation, thereby restricting their memory cell potential.

230 Allospecific CD154+T-cytotoxic memory cells predict acute cellular rejection after LTx

231 the graft and expanding in vivo; (2) central-memory cells predominated very early posttransplantation

232 In vivo, these memory cells preferentially home to lymph nodes and disp

233 nsferred naive, but not TSCM or conventional memory cells preferentially survive cyclophosphamide, th

234 , contraction, and generation of long-lived "memory" cells, processes poorly understood at the molecu

235 CD8(+) CD62L(-) KLRG1(+) CD107a(+) effector-memory cells producing IL-33.

236 tumor control but instead survived to become memory cells proficient in generating recall immunity.

237 CD4(+) T cells, while naive and less mature memory cells prove to be more resistant.

238 dary lymphoid organs, whereas in the second, memory cells recirculate between blood and nonlymphoid t

239 B-cell development was impaired, with fewer memory cells, reduced class-switching, and lower frequen

240 ansion of CD138(+) plasmablasts and T-bet(+) memory cells, respectively.

241 gly, CCR7(-/-), CD2-CCR7, and wild-type OT-I memory cells responded equally well to rechallenge infec

242 h1-specific central memory cell and effector memory cell responses highlights the importance of ident

243 selective CD28 blockade also controlled Tfh memory cell responses to KLH stimulation more efficientl

244 ytokine-driven proliferation of TCM and TSCM memory cells resulted in phenotypic conversion into TEM

245 Here we show that "pre-effector" and "pre-memory" cells resulting from the first CD8+ T cell divis

246 Stimulation of memory cells revealed enhanced transcription of "memory-

247 ction or removal of the TCR from established memory cells revealed that the induction of the TRM phen

248 or understanding the molecular regulation of memory cell states and harnessing immunological memory t

249 eplication-competent HIV in purified resting memory cell subpopulations by a limiting-dilution, quant

250 nstrate that what was believed to be a minor memory cell subset in peripheral tissues has been dramat

251 ell exhaustion especially in the CD4 central memory cell subset.

252 Analyses of memory cell subsets showed that effector memory pathways

253 9/inducible costimulator/HLA-DR frequency in memory cell subsets, as well as IFN-gamma, IL-13, IL-9,

254 impact of the allograft microenvironment on memory cell survival and activation, as well as new ther

255 Moreover, HPSCC consisted of less T-central-memory cells, T-follicular-helper cells, TGF-beta respon

256 ionately more allospecific CD154+T-cytotoxic memory cells (TcM) survived than TcM, resulting in relat

257 n and generated fewer stem cell-like central memory cells than did Myb-sufficient T cells.

258 More importantly, the memory cells that are formed do not respond properly to

259 ells (TE) as well as phenotypically distinct memory cells that are retained over time.

260 cells, including quiescent naive and central memory cells that are typically difficult to infect in v

261 survives and differentiates into long-lived memory cells that confer protection from reinfection by

262 timulation, naive T cells differentiate into memory cells that mediate antigen clearance more efficie

263 w-affinity priming is sufficient to generate memory cells that mediate potent secondary responses aga

264 T cells (T(RM)) are long-lived, nonmigratory memory cells that persist in most nonlymphoid tissues, i

265 Unlike the memory cells that typically form after successful pathog

266 harboring intact provirus was lower than in memory cells, the high abundance of naive cells in the i

267 e memory and finally from immature to mature memory cells, the latest being a no-return stage.

268 ive T cells and hence generation of adaptive memory cells, the roles of CD28 costimulation on establi

269 ay alter CCR5 expression in CD4(+) T central memory cells to promote in utero transmission of HIV-1.

270 e survival of T cells during the effector-to-memory cell transition and abolished their differentiati

271 nt for transcripts linked to tissue-resident memory cells (TRM cells), such as CD103, and CTLs from C

272 le of dense regulatory circuitry, epigenetic memory, cell type fluidity, and reuse of regulatory modu

273 henotype are the progeny of infected central memory cells undergoing antigen-driven clonal expansion

274 Recent studies suggest that some memory cells unexpectedly act as regulatory cells, promo

275 Virtual memory cells (VM) are an antigen-specific, memory phenot

276 poptotic depletion of class-switched and IgM memory cells was associated with phosphorylation of extr

277 n-free mice revealed that differentiation to memory cells was coupled to erasure of de novo methylati

278 ualities uniquely associated with protective memory cells we compared the gene expression signatures

279 oth CD3(+) CD4(+) and CD3(+) CD8(+) effector memory cells were higher, while CD25(+) Foxp3(+) T regul

280 We found that gluten tetramer-binding memory cells were rare in blood of healthy individuals.

281 Such memory cells were rare in peripheral blood, yet detectab

282 otoxic effector functions of the reactivated memory cells were reduced and the alloreactivity of DCs

283 Skin recirculating memory cells were required for optimal host defense agai

284 (+) T cells, central memory and transitional memory cells, were reported to be major reservoirs of HI

285 ed on HCV-specific CD8+CCR7+CD45RO+ (central memory) cells, whereas effector memory (CD8+CCR7-CD45RO+

286 ripheral blood contains low numbers of CD27+ memory cells which are the site of EBV persistence in he

287 ive cells, with a marked deficiency of CD27+ memory cells which lasted >12 months.

288 D8(+) T cells showed a reduced proportion of memory cells, which expressed lower levels of Tcf7, and

289 Apoptotic susceptibility of T-cytotoxic memory cells, which resist cathepsin B activation, may d

290 ike conventional T cells, differentiate into memory cells while in the thymus, our results highlight

291 An integrated memory cell with a mem-ristor and a trilayer crested bar

292 R T cells with CD28 domains yielded effector memory cells with a genetic signature consistent with en

293 the IL-17A pathway.Conclusions: RV-C induced memory cells with a lower IFN-gamma-type response than R

294 B-1b cells generated the greatest number of memory cells with higher frequencies of IgG- and CD80-ex

295 cues program recently recruited central-like memory cells with migratory potentials for their tissue-

296 d pool of terminally differentiated effector memory cells with preserved proliferative capacity, a fi

297 We are demonstrating memory cells with up to 6.5 bits of information storage

298 rganization of central- versus effector-like memory cells within the lung and how cooperation between

299 cells can sometimes acquire properties of a memory cell without encountering foreign antigen.

300 CD8(+) T cells directly convert into virtual memory cells without clonal effector T cell expansion.