ライフサイエンスコーパス: memory T-cell

1 nown to favor the generation and survival of memory T cells.

2 sociated lymphoid tissue and CD8(+) effector memory T cells.

3 icose veins preferentially contain activated memory T cells.

4 s to undergo LIP and convert into long-lived memory T cells.

5 rophages and central, stem cell and effector memory T cells.

6 is a marker for long-lived antigen-specific memory T cells.

7 lates the development of functionally mature memory T cells.

8 n, even in the absence of circulating CD8(+) memory T cells.

9 less exhausted compared with other types of memory T cells.

10 tely control differentiation of effector and memory T cells.

11 nal properties of stem cell-like and central memory T cells.

12 and minimized CD4(+)CD103(+) tissue-resident memory T cells.

13 nctional CD44(high)CD62L(high)CD8(+) central memory T cells.

14 ted in the EP by the maintenance of resident memory T cells.

15 d a reciprocal increase in the proportion of memory T cells.

16 with little to no effect on naive or central memory T cells.

17 challenge compared with high-affinity-primed memory T cells.

18 via the canonical functions associated with memory T cells.

19 omoter in skin/inflammation-seeking effector memory T cells.

20 g the differentiation of uncommitted central memory T cells.

21 tor-differentiated and mucosally distributed memory T cells.

22 enerating both circulating and skin-resident memory T cells.

23 romoting proliferation of Igm(+) B cells and memory T cells.

24 ic CTLs, in particular effector and effector memory T cells.

25 et of suppressive CD4(+)CD45RB(low) effector/memory T cells.

26 transformed T cells and Tax-immortalized CD4 memory T cells.

27 young CD25(lo) Tregs than to either naive or memory T cells.

28 cts at the level of responding NK and CD8(+) memory T cells.

29 tly activated T cells, but absent on resting memory T cells.

30 cell subsets, that is, naive, effector, and memory T cells.

31 cumulation of salivary gland tissue-resident memory T cells.

32 oxic features that is distinct from effector memory T cells.

33 es, and expanded germinal center B cells and memory T cells.

34 tribute to the maintenance of viral-specific memory T cells.

35 to differentiate into efficient effector and memory T cells able to protect us from infections.

36 X-40L, and CD70, all of which are related to memory T cell activation and maintenance.

37 IF) during establishment and reactivation of memory T cells against Gram-negative enteropathogens.

38 Memory T cells against NS1 or E proteins were poorly cro

39 ization are linked to protective efficacy of memory T cells against reinfection is unclear.

40 of CD4+ and CD8+ CD44high CD62Llow effector/memory T cells and a reduced systemic IFNgamma productio

41 Circulating memory T cells and autologous epidermal cells from sampl

42 ignificantly reduced infiltration of central memory T cells and B cells into the lungs.

43 correlation was found between CD4(+)CD44(+) memory T cells and both IL-15 of the homeostatic and IL-

44 ction of CD44(high)CD62L(low)CD8(+) effector memory T cells and CD103(high)CD8(+) tissue-resident T c

45 The proportions of both effector memory T cells and central memory T cells were reduced,

46 ith DMF treatment, especially among effector memory T cells and effector memory RA T cells.

47 tionally silent latent infections in resting memory T cells and hematopoietic stem and progenitor cel

48 tinib effectively suppresses tissue-resident memory T cells and inhibits core vasculitogenic effector

49 There was skewing in favor of memory T cells and intense autoantibody production, with

50 igher IFN-gamma production in peripheral CD4 memory T cells and lymph node-derived follicular helper

51 ssed on the surface of circulating CD45RO(+) memory T cells and most skin-infiltrating T cells.

52 amic cross-species interaction between human memory T cells and mouse macrophages in the skin and lym

53 duced frequencies of CD4(+), CD8(+), central memory T cells and MZ B cells, and an increased frequenc

54 increase in the frequency of CD8(+) central memory T cells and terminal effector T cells, a decrease

55 stem T cell, central memory T cell, effector memory T cell, and terminally differentiated effector T

56 significantly reduced IL-17A production from memory T cells, and decreased IL-17A- and IL-22-producin

57 , longevity and homeostatic proliferation of memory T cells, and most recently appreciated, clonal ex

58 effect on effector memory T cells, resident memory T cells, and recently activated T cells, inhibiti

59 ibitory signaling on activation of naive and memory T cells, and the ability of regulatory T cells (T

60 e effects on gut microbiota, SCFAs, effector memory T cells, and the acute innate immune response and

61 cluding the newly identified tissue-resident memory T cells, and whether such T cells are sensitive t

62 Memory T cells are critical for long-term immunity again

63 they can rapidly kill Ag-bearing APCs before memory T cells are engaged.

64 he ZIKV peptides recognized by DENV-elicited memory T cells are identical or highly conserved in DENV

65 find that allergen-specific tissue-resident memory T cells are maintained by IL-2 and are key driver

66 latory elements of the cytokine genes in the memory T cells are marked by activating histone modifica

67 As memory T cells are poorly controlled by 'conventional' t

68 Memory T cells are primed for rapid responses to Ag; how

69 We find that systemically induced memory T cells are restricted to the blood vessels in th

70 Islet-specific memory T cells arise early in type 1 diabetes (T1D), per

71 enes remain demethylated, demonstrating that memory T cells arise from a subset of fate-permissive ef

72 T cells without selection of CD8(+) central memory T cells as independent predictors of CRS.

73 r1 cell populations simultaneously across 23 memory T cell-associated surface and intracellular molec

74 bdoviral vectors diminishes the expansion of memory T cells, B cells do not present Ags directly.

75 aracterize the functioning of brain-resident memory T cells (bTRM) in an animal model of viral infect

76 itially reduced the numbers of LCMV-specific memory T cells, but continued MCMV persistence did not f

77 ccination route, UV-Ct-cSAP induced systemic memory T cells, but only mucosal vaccination induced eff

78 revise the paradigm of effector and central memory T cells by revealing a subset of CD8(+) memory T

79 unimmunized and OVA-immunized CD4(+)CD44(+) memory T cells by the homeostatic and inflammasome pathw

80 has been established that pathogen-elicited memory T cells can have high or low affinity for cross-r

81 Memory T cells can often respond against pathogens that

82 understood whether systemic vaccine-induced memory T cells can readily home to the lung mucosa prior

83 is stochastic response variation, individual memory T cells can serve as adult stem cells that provid

84 tuberculosis vaccine elicits a repertoire of memory T cells capable of recognizing multiple Ag85A epi

85 tissues after boosting, suggesting that the memory T cell capacity in tissues is flexible and that T

86 ral killer cells (CD69+), and PD-1+ effector memory T cells (CD45RO+).

87 functional profiling of aging antiviral CD8+ memory T cells (CD8+ TM) revealed a pervasive remodeling

88 entified a subset of influenza-specific lung memory T cells characterized as TRM cells in rhesus monk

89 to AChR, was also restricted to the CCR6(+) memory T cell compartment in the MG cohort, indicating a

90 uired chronic phenotype transitions into the memory T cell compartment.

91 To assess the dynamics of Ag-specific memory T cell compartments in the context of filarial in

92 urthermore, studies on human CD4(+) effector memory T cells confirmed demethylation within FUT7 corre

93 s were observed between activated B-cell and memory T-cell counts (P < .02).

94 mory T cells by revealing a subset of CD8(+) memory T cells defined by intermediate levels of express

95 expansion of memory stem T cells and central memory T cell-derived T cells compared with IL-2.

96 ng a long-standing debate centred on whether memory T cells develop from effector cells or directly f

97 However, MAVS is dispensable for memory T cell development and host protection during sec

98 tor T cell differentiation, and potentiating memory T cell development.

99 ly defective PD-1(hi) effectors; and rescues memory T-cell development and responsiveness to IL-7-dep

100 argets, and productive infection of CCR7(hi) memory T cells did not alter chemotaxis to CCL19 and CCL

101 ion of positive histone modifications during memory T cell differentiation.

102 mproved T cell expansion and favored central memory T cell differentiation.

103 TH1, TH17, and CD8(+) memory T-cell differentiation was significantly reduced,

104 of naive T cell, memory stem T cell, central memory T cell, effector memory T cell, and terminally di

105 these strategies fail to control pathogenic memory T cells efficiently and to improve long-term tran

106 Central memory T cells expanded in the presence of HLA-DR(+) NK

107 ncreases the efficacy of mATG in controlling memory T cell expansion and significantly extends heart

108 efore 2 years of age showed smaller effector memory T-cell expansions than those infected between 2 a

109 and Epstein-Barr virus (EBV) induce effector memory T-cell expansions, which are variable and potenti

110 Memory T cells expressing stem cell-like properties have

111 may be required for optimum CD4(+) CD45RO(+) memory T cell expression.

112 n the absence of self-pMHC interactions, CD8 memory T cells fail to undergo bystander activation upon

113 many of these responses without suppressing memory T cell formation and induced additional changes i

114 a long-lived effector fate at the expense of memory T cell formation.

115 The frequency of CCR6(+) memory T cells from MG patients proliferating in respons

116 usage compared with gluten tetramer-binding memory T cells from patients.

117 In RA, RBPJ expression is elevated in memory T cells from RA patients compared with control su

118 ures to analysis of islet Ag-reactive CD4(+) memory T cells from the blood of T1D and HC individuals

119 reas off-target vaccine responses activating memory T cells from the related herpesvirus Epstein-Barr

120 mory; however, how innate immunity regulates memory T cell function remains obscure.

121 n wild-type animals, and even virus-specific memory T cells generated by prior immunization could not

122 iescence, T cell subset differentiation, and memory T cell generation.

123 These characteristics of memory T cells have mainly been studied during viral inf

124 9, 95% CI 0.80-0.98; p = 0.02) and activated memory T cells (HR 0.88, 95% CI 0.80-0.97; p = 0.01) wer

125 eration and persistence of allergen-specific memory T cells in asthmatic patients and translate these

126 We quantified TH1/TH2/TH17 CD4 memory T cells in blood and lymph nodes of patients with

127 s, we sought to determine the profile of CD4 memory T cells in blood and secondary lymphatic tissues

128 on of CD45 and CD127 suggest the presence of memory T cells in both twins, but effector T cells only

129 tly related to larger expansions of effector memory T cells in children, suggesting that other mechan

130 We show that memory T cells in kidney transplant patients, in particu

131 ce, STAT5B is a crucial regulator of RICD in memory T cells in mice and humans.

132 issue-retention and equilibration for CD4(+) memory T cells in skin, which is altered by infection an

133 activation of CD4(+) and CD8(+) effector and memory T cells in the cord blood compared with controls.

134 induction of mycobacteria-specific resident memory T cells in the lung by aerosol administration, or

135 TH2 effector cells in the lungs and central memory T cells in the mediastinal lymph nodes.

136 nce in failing hearts, and with expansion of memory T cells in the spleen.

137 MCs or coculture systems were used to detect memory T cells in treated patients.

138 ent of optimal expression of CD4(+)CD45RO(+) memory T cells in unimmunized and OVA-immunized BALB/c m

139 Memory T cells in white adipose tissue expressed a disti

140 reas adult tissues contain a predominance of memory T cells, in pediatric blood and tissues the main

141 iting, had higher densities of Th1, effector-memory T cells, in situ proliferating T cells, and inhib

142 cumulated large numbers of pathogen-specific memory T cells, including tissue-resident cells.

143 loantigens and are able to generate effector/memory T cells independently from CD4+ T cells.

144 ) T cells and retain them as tissue-resident memory T cells, independently of local infection, inflam

145 sociated lncRNA abrogates IFNG expression by memory T cells, indicating these lncRNAs have biologic f

146 ectin ligands (E- and P-ligs) guide effector memory T cells into skin and inflamed regions, mediate t

147 Concurrent redistribution of memory T cells into the circulation not only leads to ex

148 The selective recruitment of memory T cells into these lymphoid structures occurred i

149 The long-term maintenance of memory T cells is essential for successful vaccines.

150 establish clonal derivatives as circulating memory T cells is less understood.

151 ory reflex arc involving the vagus nerve and memory T cells is necessary for resolution of acute infl

152 s, a population of terminally differentiated memory T cells, is one of the most consistent immunologi

153 previously identified as controlling central memory T-cell levels.

154 cell epitopes, establishing antigen-specific memory T-cell lines for identifying CD8(+) and CD4(+) T-

155 fferentiation state (naive T cells < central memory T cells < effector memory T cells < T effector me

156 T cells < central memory T cells < effector memory T cells < T effector memory RA(+) cells).

157 utional component for the "rebound model" of memory T cell maturation.

158 fferentiation, but minimally impacted CD8(+) memory T cell maturation.

159 orly controlled by 'conventional' therapies, memory T-cell mediated attack is a substantial challenge

160 long-term Ag-specific unresponsiveness in a memory T cell-mediated inflammatory skin model.

161 Consequently, CD8(+) memory T cell-mediated targeting of islet-expressed anti

162 -FoxO1 axis as a regulator of resting CD8(+) memory T cell metabolism and activity in humans.

163 CD8CD28 end-stage terminally differentiated memory T cells/muL rejected, median pretransplant values

164 ensure lifelong immunocompetency, naive and memory T cells must be adequately maintained in the peri

165 When cultured in the presence of memory T cells, naive-derived T cells show increased dif

166 he HA-1 TCR CD8(+) T cells and includes only memory T cells; naive T cells are excluded to limit the

167 ells, and an increased frequency of effector memory T cells, neutrophils, follicular, and MZ P B cell

168 Bim-mediated contraction and do not increase memory T cell numbers.

169 Naive and central memory T-cell numbers were not affected, nor were anti-t

170 In the L-NAME/high-salt model, memory T cells of the kidney were predominant sources of

171 dily in the central memory (CM) and effector memory T cells over 48 weeks.

172 was a higher percentage of terminal effector memory T cells (P = 0.03) and LPS-stimulated ex vivo pro

173 enhancing expansion, effector function, and memory T-cell persistence.

174 gammadelta T cells with a tissue resident memory T cell phenotype (CD69(+)CD103(+)) were expanded

175 a short-lived effector rather than effector memory T cell phenotype postinfection and expressed high

176 stent with a central memory or recirculating memory T cell phenotype.

177 pecific, IL-12-dependent, and induces innate memory T cell phenotypic markers.

178 t compromise naive, regulatory, or quiescent memory T-cell pools, and had a modest nonimmune toxicity

179 of the latent HIV-1 reservoir in the CD4(+) memory T cell population prevents viral eradication with

180 rtheless, given the constant exposure of the memory T cell population to specific antigen or bystande

181 Both the quantity and the quality of the memory T-cell population must be maintained.

182 tigate the impact of TCR-priming affinity on memory T cell populations following a graft rechallenge.

183 ls was required for the optimal formation of memory T cell populations, in particular TRM cell popula

184 ponses and adoptive transfer of IAV-specific memory T cell populations, we find that without IL-6, CD

185 er in effector relative to naive and central memory T-cell populations, and activation of resting T c

186 nd induction of unresponsiveness in targeted memory T-cell populations.

187 ctor T cells die, and only a small number of memory T cell precursors (TMPs) survive to form a pool o

188 ute to the generation of CD8(+) effector and memory T cell precursors.

189 ransplant lymphocyte depletion induces rapid memory T cell proliferation and only modestly prolongs a

190 Most importantly, active memory T cell proliferation before therapy predicted SVR

191 is cohort demonstrated that increased CD8(+) memory T-cell proliferation, higher granzyme B productio

192 Tissue-resident memory T cells provide local immune protection in barrie

193 However, a subset of effector memory T cells re-expresses CD45RA (termed TEMRA) after

194 ggest that white adipose tissue represents a memory T cell reservoir that provides potent and rapid e

195 ltogether, we believe that allergen-specific memory T cells reside and function in the lung and airwa

196 gly, S1P had the opposite effect on effector memory T cells, resident memory T cells, and recently ac

197 t expansions of CD27(-) and CD27(+) effector memory T cells, respectively.

198 Memory T cells respond rapidly to repeated antigen expos

199 the first full-breadth analysis of the human memory T cell response using a synthetic peptide library

200 ost animals associated with a tumor-specific memory T-cell response.

201 These findings indicate that pathogenic memory T cell responses are controlled by both CD28 and

202 As all memory T cell responses are encoded in the common format

203 Our data show that memory T cell responses elicited by prior infection with

204 We find that memory T cell responses elicited by prior infection with

205 f the alloimmune and single antigen-specific memory T cell responses in the absence of immunosuppress

206 Collectively, these results suggest that CD8 memory T cell responses to nonpersistent viruses like IA

207 iptional repression of genes associated with memory T cell responses.

208 rapy effectively terminates antigen-specific memory T-cell responses and this can alleviate destructi

209 timately developed long-term, polyfunctional memory T-cell responses to Lassa virus.

210 permits a more meaningful monitoring of CD8 memory T-cell responses to viral infections and tumors a

211 Among these, memory T cells serve a sentinel role to protect against

212 Transcriptomic analysis of rs874040(CC) memory T cells showed a repression of canonical Notch ta

213 Ag-specific CD8 T cells display a canonical memory T cell signature associated with long-lived memor

214 inued MCMV persistence did not further erode memory T cells specific to LCMV.

215 Unlike memory T cells, spontaneous Ab secreting cells and memor

216 lectivity and potency against effector human memory T cells (subnanomolar to picomolar EC50 values).

217 It is now clear that there exists a distinct memory T cell subset that is absent from blood but found

218 T memory stem cells (TSCM) are a unique memory T cell subset with enhanced self-renewal capacity

219 ly related to a resting PD1(+)ICOS(-) CD4(+) memory T cell subset.

220 n and suggest that S1P promotes retention of memory T cell subsets in secondary lymphoid organs, via

221 urified naive, stem cell memory, and central memory T cell subsets results in superior persistence an

222 t-cSAP vaccination generated two synergistic memory T cell subsets with distinct migratory properties

223 and the ability to differentiate into other memory T cell subsets, such as central and transitional

224 peripheral blood stem cell grafts (naive and memory T-cell subsets, B cells, regulatory T cells, inva

225 nsity of infiltrating mature DC and effector memory T-cell subsets, suggesting that CRT triggers the

226 ), but the mechanisms by which IL-7 controls memory T cell survival, particularly metabolic fitness,

227 Reduced memory T-cell survival and altered memory cell different

228 Memory T cells sustain effector T-cell production while

229 During these challenges effector memory T cells (T(EM)) accumulated in the kidney and bon

230 naive recent thymic emigrants, with effector memory T cells (T(EM)) found only in the lungs and small

231 rapidly seeded uterine mucosa with resident memory T cells (T(RM) cells).

232 ll subsets, such as central and transitional memory T cells (TCM and TTM, respectively).

233 munizations to rapidly expand CD8(+) central memory T cells (TCM) during the acute phase of the prima

234 memory T cells (Tem), CD4(+)PD-1(+) central memory T cells (Tcm), Tcm PD-1 expression, and neutrophi

235 onitored by Immuno-PET imaging human central memory T cells (TCM), which were transgenic for a myeloi

236 conformation, compared with <20% in central memory T cells (TCM).

237 level of SIV DNA in CD4(+) TSCM and central memory T cells (TCM-) did not significantly change.

238 ity and proliferative capacity than effector memory T cells (TEFF) and, therefore, polarizing vaccine

239 4(high) CCR7(low) CD62L(low) CD8(+) effector memory T cells (TEM cells) in ASYMP individuals than SYM

240 Effector memory T cells (TEM) are less capable of inducing graft-

241 NK cells and both CD4(+) and CD8(+) effector memory T cells (TEM) in blood and tissues, with little t

242 We show in mouse effector memory T cells (TEM) that >50% of lymphocyte-specific pr

243 ) natural killer cells (NK), CD4(+) effector memory T cells (Tem), CD4(+)PD-1(+) central memory T cel

244 viability, and cytotoxic action of effector memory T cells (TEM).

245 on of terminally differentiated CD8 effector memory T cells (TEMRA) in peripheral blood during the fi

246 ys influence the generation of skin-resident memory T cells that arise from a polyclonal repertoire o

247 g to generation of CD4 effector and effector memory T cells that contribute to protection.

248 uncover a multi-organ web of tissue-resident memory T cells that functionally adapt to their environm

249 ure promoted the outgrowth of CD8(+) central memory T cells that had significantly enhanced respirato

250 r CD8(+) T cells and increases the number of memory T cells that participate in the recall protection

251 effector T cells that clear the pathogen and memory T cells that persist long-term and provide height

252 ector T cells that provide acute defense and memory T cells that provide long-lived immunity.

253 med that latent HIV-1 resides exclusively in memory T cells that recognize rare antigens.

254 ficient for the activation of both naive and memory T cells, the memory cells are capable of producin

255 mplications for manipulating tissue-resident memory T cells through vaccination and open up new lines

256 Memory T cells (TM) play a prominent role in protection

257 Understanding the mechanisms of CD4 memory T cell (Tmem) differentiation in malaria is criti

258 blocking PD-1 can reprogram TEX into durable memory T cells (TMEM) is unclear.

259 n about the features of resting or exhausted memory T cells (Tmem), little is known about the functio

260 Memory T cells (Tmem), particularly those resistant to c

261 (TMPs) survive to form a pool of long-lived memory T cells (TMs).

262 found that, in contrast to naive and central memory T cells (TN and TCM), hypoxia enhances the prolif

263 Nevertheless, the ability of memory T cells to elicit well characterized manifestatio

264 m of functional states ranging from effector memory T cells to exhaustion.

265 TRIF activated memory T cells to facilitate local neutrophil influx and

266 ry peptide, is released by vagally modulated memory T cells to suppress the expansion of MDSCs throug

267 monstrate that the rs874040(CC) allele skews memory T cells toward a pro-inflammatory phenotype invol

268 splays a biased central memory phenotype and memory T cell transcriptional profile, innate-like prope

269 sulitic lesions to display a tissue resident memory T cell (TRM) (CD8(+)CD69(+)CD103(+)) phenotype in

270 CD8(+)/CD103(+) tissue-resident memory T cells (TRM cells) accumulate in several human s

271 of pathogen-specific CD8(+) tissue-resident memory T cells (TRM cells) in the lamina propria.

272 rhans cells (LCs) and CD8(+) tissue-resident memory T cells (TRM cells) require active transforming g

273 nstrate that CD4(+) and CD8(+) skin-resident memory T cells (TRM cells), which are responsible for lo

274 ed by a long-lived subset of tissue-resident memory T cells (Trm cells).

275 These tissue-resident memory T cells (TRM) are preferentially expanded in pati

276 Tissue-resident memory T cells (TRM) have been shown to afford superior

277 Tissue-resident memory T cells (TRM) persist at sites of prior infection

278 udies identifying protective tissue-resident memory T cells (Trm) suggest an alternative paradigm bas

279 adult mice, lung-localized, tissue-resident memory T cells (TRMs) mediate optimal protection to resp

280 of human resting naive, central and effector memory T cells using ChIP-Seq and found that unlike the

281 frequency of Pf-specific polyfunctional CD4 memory T cells was associated with protection.

282 requency of influenza nucleoprotein-specific memory T cells was detected in the lung at the "contract

283 ence of potentially pathogenic skin resident memory T cells well beyond clinically inflamed lesions.

284 107(a/b+)CD44(high)CD62L(low)CD8(+) effector memory T cells were detected in ASYMP individuals and we

285 HCMV-specific memory T cells were investigated in the second month aft

286 CD8CD28 end-stage terminally differentiated memory T cells were measured pretransplantation and post

287 Memory T cells were preferentially found in the lower tr

288 of both effector memory T cells and central memory T cells were reduced, whereas naive T cells incre

289 ened activation of SMX-NO-specific naive and memory T cells, whereas blockade of TIM-3 produced no ef

290 lls expressed CD69, consistent with resident memory T cells, whereas the remaining CCR7(hi) CD4 T cel

291 r KCa3.1 on autoantigen-experienced effector memory T cells, whether Kv1.3 is required for their indu

292 cept was predominantly mediated by cytotoxic memory T cells, which are less susceptible to costimulat

293 Formation of memory T cells, which requires the costimulatory molecul

294 CD4(+) and CD8(+):Treg ratios, and increased memory T cells while decreasing naive T cells.

295 finity priming elicited fully differentiated memory T cells with a CD45RB(hi) status.

296 e frequency of these CD8(+) T cells, called 'memory T cells with a naive phenotype' (TMNP cells), inc

297 at the majority of cells are tissue resident memory T cells with high levels of CD69 and CD103 expres

298 gs demonstrate that islet Ag-reactive CD4(+) memory T cells with unique Ag specificities and phenotyp

299 Although memory T cells within barrier tissues can persist as per

300 in an increased proportion of CD4(+) central-memory T cells within the draining lymph nodes following