ライフサイエンスコーパス: memory cell

1 electrodes confining the resistive switching memory cell.

2 urations that can be utilized for a multibit memory cell.

3 ls and their differentiation into functional memory cells.

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

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

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

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

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

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

10 not complete differentiation programs toward memory cells.

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

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

13 entary organic circuits, and two nonvolatile memory cells.

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

15 mpaired proliferation and reduced numbers of memory cells.

16 ignaling impairs the development of effector memory cells.

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

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

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

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

21 d differential methylation between naive and memory cells.

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

23 for the development of these unconventional memory cells.

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

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

26 efects in expansion and differentiation into memory cells.

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

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

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

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

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

32 of atopy showed increases in circulating Th2 memory cells.

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

34 ) and CD8(+) and mostly effector and central memory cells.

35 to generate a pool of mature, MCMV-specific memory cells.

36 like memory cells, including tissue-resident memory cells.

37 e via mature/naive to Ig-secreting cells and memory cells.

38 portion of CD8(+) T cells differentiate into memory cells.

39 tribute to adaptive immunity as effector and memory cells.

40 differentiation and/or survival of effector memory cells.

41 owing the resolution of infection and become memory cells.

42 D4 regulatory T cells, CD4 Th cells, and CD8 memory cells.

43 ave a severe defect in generating protective memory cells.

44 bset, intermediate between naive and central memory cells.

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

46 the development and survival of effector and memory cells.

47 of effector cells to functionally competent memory cells.

48 atly enhanced generation of CD62L(+) central memory cells.

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

50 ty of activated T cells to become long-lived memory cells.

51 ctor in promoting the differentiation of Th1 memory cells.

52 se cells was more characteristic of effector memory cells.

53 creased formation of polyfunctional lymphoid memory cells.

54 arly Tfh cells can progress to robustly form memory cells.

55 and would normally be classified as effector memory cells.

56 most HIV DNA and RNA were found in effector memory cells.

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

58 to have multiplexed quantum memory with many memory cells.

59 the transcriptional program associated with memory cells.

60 nes, thereby accelerating the development of memory cells.

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

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

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

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

65 pirical and more predictive design of future memory cells.

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

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

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

69 and functional characteristics of long-lived memory cells.

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

71 T cell response and its differentiation into memory cells.

72 development of circulating and lung-resident memory cells.

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

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

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

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

77 CD4+ memory cells activated by allogeneic rapa-ECs became hyp

78 and differentiation into long-lived central memory cells after adoptive transfer.

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

80 ntigen-driven expansion to become long-lived memory cells after mouse cytomegalovirus (MCMV) infectio

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

82 and cytokine secretion from allogeneic CD4+ memory cells, an effect mimicked by shRNA knockdown of m

83 , 2-deoxyglucose, enhanced the generation of memory cells and antitumor functionality.

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

85 ced the excessive numbers of CD4(+) effector/memory cells and B cells.

86 (+) T cells that allows differentiation into memory cells and cement Bcl-2 as a critical factor for T

87 gs in murine skin with properties typical of memory cells and defined this population as memory Tregs

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

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

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

91 by higher proportions of circulating CD4(+) memory cells and lower proportions of naive cells, would

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

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

94 Increased numbers of switched memory cells and plasmablasts in combination with clonal

95 trating B lymphocytes (TIL-B), both switched memory cells and plasmablasts were expanded, as compared

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

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

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

99 display phenotypic and functional traits of memory cells and provide essential protection against in

100 CD8 T cell differentiation into effector and memory cells and provides an approach to optimize vaccin

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

102 hare properties of both central and effector memory cells and reside in LN based on previously undesc

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

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

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

106 mors, as well as Th1, Th2, and Th17 effector memory cells and Tregs.

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

108 s preferentially differentiated into central memory cells and were capable of mounting a potent secon

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

110 se of sCD30 was attributed mainly to central memory cells, and neutralization of IFN-gamma (P<0.001)

111 were functionally distinct from conventional memory cells, and served as precursors of central memory

112 ung, compared to effector memory and central memory cells, and shortly after influenza virus infectio

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

114 Memory cells are a critical component of protective immu

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

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

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

118 A greater understanding of how memory cells are generated will inform of ways to improv

119 Memory cells are heterogeneous, including not only memor

120 ne differentiation of naive CD8 T cells into memory cells are not well understood.

121 Immune memory cells are poised to rapidly expand and elaborate

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

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

124 Memory cells are the products of immune responses but al

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

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

127 t phenotypically and functionally similar to memory cells arising as a result of homeostatic prolifer

128 independent of previously identified innate memory cells, arising as a result of their response to I

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

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

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

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

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

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

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

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

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

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

139 These memory cells can mount a faster and stronger response wh

140 gram that is essential to forming long-lived memory cells capable of immune reactivation.

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

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

143 Inducible proliferation of TH17(22) with memory cell characteristics is seen in the lungs of pati

144 ctivated CD8 T cells, in a specific phase of memory cell commitment, after activation but before term

145 er levels of naive cells and lower levels of memory cells compared with African-Americans and Hispani

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

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

148 emory, and postchallenge CD8(+) transitional memory cells correlated with control of viremia.

149 A low frequency of 85A-specific memory cells could be revealed by in vivo or in vitro bo

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

151 chemotactic cues that further increase local memory cell density.

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

153 nts a technological breakthrough towards new memory cell designs.

154 stimulate differentiation into effector and memory cells differed.

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

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

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

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

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

160 environmental cues for clonal expansion and memory cell differentiation.

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

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

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

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

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

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

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

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

169 However, these reactivated memory cells failed to survive.

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

171 T cell to undertake either an effector or a memory cell fate.

172 mmitment of naive CD8 T cells to effector or memory cell fates can occur after a single day of antige

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

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

175 tially survived in comparison with all other memory cells following elimination of antigen, and stabl

176 unction, to generate effector and persistent memory cells for tumor eradication, and to prevent lung

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

178 a as an important regulator of the number of memory cells formed during infection.

179 ter VACV immunization depends on the initial memory cell frequency and ability of expanded secondary

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

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

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

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

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

185 asing oligoclonality but also interfere with memory cell generation.

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

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

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

189 tionally heterogeneous; subsets of naive and memory cells have different functional properties, and a

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

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

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

193 e number of CMV-specific CD4(+) IFN-gamma(+) memory cells in BAL was significantly increased in LTRs

194 cells were CD45RO(+)CCR7(-)CD127(-) effector memory cells in exposed health care workers and in patie

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

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

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

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

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

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

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

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

203 ing, which were preferentially effector-like memory cells, including tissue-resident memory cells.

204 Stacking nonvolatile memory cells into a three-dimensional matrix represents

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

206 to survive the contraction period to become memory cells is incompletely understood.

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

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

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

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

211 th cell subsets, we showed that transitional memory cells may not be a durable reservoir in patients

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

213 -1(+)CXCR5(+)CD4(+) T cells that are resting memory cells most related to bona fide GC Tfh cells by g

214 Each memory cell needs to be individually addressable and ind

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

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

217 d a corresponding 4-fold reduction in CD4(+) memory cell number.

218 155 exhibited severely impaired effector and memory cell numbers in both lymphoid and nonlymphoid tis

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

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

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

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

223 tatic proliferation without development of a memory cell phenotype.

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

225 possibly downstream of IL-21R, regulates the memory cell pool.

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

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

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

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

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

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

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

233 l differentiation, thereby restricting their memory cell potential.

234 CD4 and CD8 T cells share core aspects of a memory cell precursor gene expression program involving

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

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

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

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

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

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

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

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

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

244 Furthermore, the adoptively transferred memory cells responded to tumor rechallenge exerting lon

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

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

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

248 The majority of mutated VH4-34 memory cells retain the HP, thereby suggesting selection

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

250 arts and antigen rechallenge, TSC1-deficient memory cells showed moderate defects in expansion but no

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

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

253 romotes abortive infection of this important memory cell subset.

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

255 9/inducible costimulator/HLA-DR frequency in memory cell subsets, as well as IFN-gamma, IL-13, IL-9,

256 lity of tissue-specific factors that enhance memory cell survival may collectively account for the ti

257 ility of tissue-specific factors may enhance memory cell survival.

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

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

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

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

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

263 or cells that mediate acute host defense and memory cells that provide long-lived immunity, but the f

264 ated by IL-15, and produces Ag-inexperienced memory cells that retain the capacity to respond to nomi

265 Unlike the memory cells that typically form after successful pathog

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

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

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

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

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

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

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

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

274 Generation of the memory cells was CD4 T cell dependent and required IL-21

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

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

277 Higher memory cells were associated with coronary artery calcif

278 Lower naive/higher memory cells were associated with interleukin-6 levels.

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

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

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

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

283 f perforin and the generation of short-lived memory cells, whereas stimulation with 4-1BB agonists fa

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

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

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

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

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

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

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

291 onstitutively populated with CD4(+) effector memory cells with a T-cell receptor repertoire specific

292 survival but that Wnt high effectors yielded memory cells with enhanced proliferative potential and s

293 following adoptive transfer and rechallenge, memory cells with high Wnt levels displayed increased re

294 ed increased recall expansion, compared with memory cells with low Wnt signaling, which were preferen

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

296 ects, this therapy altered the metabolism of memory cells with self-renewing phenotype and provided a

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

298 ional CD4 T cell compartments, such as naive/memory cells, with shallow, multiple identifier-based HT

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

300 andom migration effectively constrains these memory cells within the region of skin in which they for