ライフサイエンスコーパス: CTL

1 CTLs achieve this by forming an immunological synapse wi

2 CTLs can directly kill tumor cells in a contact-dependen

3 CTLs engaging cognate targets accelerate the recruitment

4 CTLs release cytotoxic proteins such as granzymes and pe

5 Under 5% O(2), CTL TB and EOPE TB lines did not differ, but, under hype

6 We investigate the clonal repertoire of 29 CTL responses against 23 HIV-1 epitopes longitudinally i

7 as enriched in cells expressing PD-1, TIM-3, CTL-associated protein 4 (CTLA-4), or B and T lymphocyte

8 ly correlated with the NIRF signals of Cy5.5-CTLs at targeted tumor tissues in the early stage.

9 ith the intensity of NIRF signals from Cy5.5-CTLs at tumors after 2-3 days post-injection.

10 The labeling efficiency of Cy5.5-CTLs could be readily controlled by changing concentrati

11 Importantly, Cy5.5-CTLs presented the strong NIRF signals in vitro and they

12 The Cy5.5-CTLs showed different therapeutic responses in E.G-7 tum

13 deficient mice, intravenously injected Cy5.5-CTLs were clearly observed at targeted solid tumors via

14 ese different therapeutic responses of Cy5.5-CTLs were highly correlated with the NIRF signals of Cy5

15 stry, resulting in Cy5.5-labeled CTLs (Cy5.5-CTLs).

16 ve immunotherapeutic approaches with BCR-ABL CTLs in Ph(+) ALL.

17 molecules, which is important for activating CTL against viral infections and tumors.

18 llorecognition as an approach for activating CTL capable of recognizing weak or self-antigens in the

19 tiproliferative effect of IFNgamma might aid CTLs in tumor control.

20 These data highlight that not all CTLs expressing PD-1 are dysfunctional; on the contrary,

21 FLs) of species have been proposed alongside CTLs, to better assess the sublethal effects of rising t

22 Through the mapping of cytokine- and CTL-based genetic interactions, together with in vivo CR

23 trengthened the CTL epitope presentation and CTL responses.

24 SBTx and prompt escalation to rituximab and CTL is recommended.

25 sion of individual genes between EOPE TB and CTL TB under 20% O(2), but, a weighted correlation netwo

26 phenotype capable of Th1, follicular Th, and CTL functionalities, yet they are unable to be infected

27 monitoring of PD-L1 positive tumor cells and CTLs with cellular resolution by non-invasive NIR-IIb li

28 egrees of clustering between tumor cells and CTLs, and between tumor cells and HLA-DR(+) macrophages,

29 were secreted per cell for both NK cells and CTLs, but NK cell SMAPs were larger.

30 -gamma secreting total T cells, T-helper and CTLs against both H1N2 and H1N1 SwIV.

31 ression and altered infiltration of TAMs and CTLs as evidenced by immunohistochemical and flow cytome

32 Newly arriving CTLs augment the chemotactic signal, further acceleratin

33 and its recognition by specific autoreactive CTLs during inflammation.

34 from band edges) from DFT total energy-based CTL and separate DFT + GW calculations.

35 herichia coli (E. coli) were not affected by CTL or APS diets.

36 endence and MxB sensitivity likely driven by CTL escape.

37 cancer-cell-intrinsic evasion of killing by CTLs and we highlight the importance of these effects wi

38 types associated with escape from killing by CTLs.

39 am of CTL epitopes can also be recognized by CTLs, potentially through aberrant translation.

40 a more potent effector function, as shown by CTLs, in vivo assays.

41 onstrate that adoptively transferred (5M)CAR-CTLs can mitigate type I diabetes by targeting autoimmun

42 lls and cytotoxic T helper (T(H)) cells (CD4-CTLs) responding to SARS-CoV-2 and reduced proportion of

43 tivation and expansion of polyfunctional CD8 CTLs and tumor regression.

44 Y-241 enhances autologous MM-specific CD8(+) CTL activity.

45 as increases pDC-induced MM-specific CD8(+) CTL and NK cell activity against autologous tumor cells.

46 action of antigen-specific cytotoxic T cell (CTL) in vivo results in the emergence of resistant cance

47 sists despite HIV-specific cytotoxic T cell (CTL) responses.

48 toantigen epitopes implicated in CD8 T cell (CTL)-mediated beta-cell destruction in type 1 diabetes (

49 g of the TME and unleashed cytotoxic T cell (CTL)-mediated tumor eradication.

50 minimal effect on the cytotoxic CD8 T-cell (CTL) mediated response.

51 degradation and generate cytotoxic T cells (CTLs) against N peptide.

52 enhances the activity of cytotoxic T cells (CTLs) could identify potential targets for immunotherapy

53 in (OVA) antigen-specific cytotoxic T-cells (CTLs) were incubated with N-azidoacetyl-D-mannosamine-te

54 During CMV-CTL monitoring using mutated HLA/CMV tetramers selective

55 ity T cells, we observed coappearance of CMV-CTLs with low (CMV tet(low) CTLs) and high tetramer bind

56 These CTL-derived vesicles contain CTL proteins and exhibit markers and size profiles consi

57 significantly higher rates of contralateral (CTL) TLH (p = 0.016).

58 In contrast, CTL responses to DC-derived exosomes were significantly

59 ight finisher diets consisting of 4 control (CTL) diets based on SBM with different crude protein (CP

60 lysis were randomized into either a control (CTL, n = 25) and RT group (RTG; n = 30).

61 ed from umbilical cords of EOPE and control (CTL) pregnancies.

62 ed Langendorff-perfused hearts from control (CTL) and heart failure (HF) mice (HF induced by transaor

63 ifferent between the ZO-1cKO versus control (CTL) mice, basally in young or aged mice, or even when h

64 upon antigen stimulation of ARPC1B-deficient CTLs, leading to a progressive loss of CD8+ T cells.

65 locked at an early stage in Flower-deficient CTLs and is rescued to wild-type level by reintroducing

66 hesize that the slow motility mode describes CTLs creating channels through the collagen matrix by de

67 rs and that the fast motility mode describes CTLs moving within these channels.

68 llular Potts model, in both cases describing CTLs that kill target cells.

69 ted with control of HIV in that the dominant CTL response is Env specific, not Gag specific.

70 nsion of E75-specific cytotoxic T cells (E75-CTL).

71 o reasons: First, the killing signal of each CTL gets diluted over several targets and because this d

72 eic, off-the-shelf bank of 330 GMP-grade EBV-CTL lines from specifically consented healthy HCT donors

73 I BL xenografts, decitabine followed by EBV-CTLs results in T-cell homing to tumors and inhibition o

74 lysis by EBV-specific cytotoxic T cells (EBV-CTLs).

75 y) can also induce remissions if initial EBV-CTLs are ineffective.

76 ed EBV-specific cytotoxic T-lymphocytes (EBV-CTLs) can eradicate EBV-associated lymphomas (EBV-PTLD)

77 ycles consisted of 3 weekly infusions of EBV-CTLs and 3 weeks of observation.RESULTSEBV-CTLs did not

78 peutics licensed the bank of third-party EBV-CTLs from Memorial Sloan Kettering Cancer Center in June

79 median of 2 cycles.CONCLUSIONThird-party EBV-CTLs of defined HLA restriction provide safe, immediatel

80 iled rituximab therapy, with third-party EBV-CTLs.

81 ith POD after a first cycle who received EBV-CTLs from a different donor achieved CR or durable PR (6

82 Secondary treatment with EBV-CTLs restricted by a different HLA allele (switch therap

83 RPM-induced early effector CTL also contributed to the endogenous antiviral respons

84 a few days, RPM induced very early effector CTL of a distinct phenotype (Ly6A/E(+) Ly6C((+)) KLRG1(-

85 d, whereas cDC1 induced short-lived effector CTL that eventually cleared the virus.

86 for both the normal accumulation of effector CTLs following acute viral infection and the protective

87 ) to selectively induce more potent effector CTLs derived from naive, rather than memory, CD8(+) T ce

88 To elicit CTL responses, epitope vaccines go through an epitope pr

89 2 and AMPK as therapeutic targets to enhance CTL activity.

90 V-infected cells was accompanied by enhanced CTL-mediated clearance of infected cells comparable to g

91 In vivo, inhibition of PCs enhanced CTL infiltration in colorectal tumors and increased tumo

92 of BCL-2 antagonism as a means of enhancing CTL immunotherapy in other settings, such as cancer.

93 observed in clones did not have more escaped CTL epitopes than intact proviruses observed as singlets

94 nd the ability of HIV-1 to rapidly establish CTL escape variants presents major hurdles toward this g

95 oromethylketone repressed PD-1 and exhausted CTLs via induction of T-cell proliferation and apoptosis

96 We also observe that pre-existing CTLs within the tumor are sufficient and essential for s

97 SMAPs were rapidly released from CTLs and were autonomously cytotoxic.

98 upramolecular attack particles (SMAPs), from CTLs to target cells.

99 wledge, that both CMV tet(low) and tet(high) CTLs are functional effector T cells differing by prolif

100 CMV tet(low) and tet(high) CTLs had an identical effector memory CD45RA(-)CCR7(-) a

101 sis revealed that CMV tet(low) and tet(high) CTLs use different TCRs.

102 Ls) and high tetramer binding (CMV tet(high) CTLs) in 53/115 CMV IgG(+) patients stem cell transplant

103 uring multistage killing saturates at higher CTL and target cell densities.

104 How CTLs escape unscathed remains a mystery.

105 However, how CTLs regulate the termination of granule secretion remai

106 lyze migration trajectories of primary human CTLs.

107 thogens is generally accomplished by immense CTL expansion and activation, which can destroy infected

108 Importantly, CTL activated in this manner can break self-tolerance by

109 Genetic stabilization of IFNAR1 improved CTL survival and increased the efficacy of the chimeric

110 ion and apoptosis inhibition, which improved CTL efficacy against microsatellite instable and microsa

111 In CTL hearts, 1.4% of myocytes were poorly synchronized wi

112 we reveal independent emergent behaviour in CTL populations attacking tumour masses.

113 ealed that Tregs were critically involved in CTL tolerance.

114 ates were significantly lower in IMB than in CTL (-14% +/- 5%; P < 0.01) and postprandial MitoPS rate

115 ater extent in IMB (-27.9% +/- 4.4%) than in CTL (-14.3% +/- 4.4%; P = 0.043) with no difference betw

116 ates were significantly lower in IMB than in CTL (-22% +/- 4%; P < 0.01) in both LEU and PLA.

117 III were significantly lower in IMB than in CTL (P < 0.05), with no differences between groups.

118 ed two gene modules (CTL4 and CTL9) that, in CTL TB, were significantly linked to extent of TB invasi

119 nological synapse regulate cortical actin in CTLs, providing a potential mechanism through which CTLs

120 tress, decompresses blood vessels, increases CTL infiltration, and decreases immunosuppression in mur

121 e that contains the virus until cDC1-induced CTL are available to eliminate it.

122 ing vaccination strategies aimed at inducing CTL.

123 We quantified whether infiltrating CTLs are capable of controlling tumors through only dire

124 in response to 20 g milk protein ingestion (CTL: -10% +/- 8%; IMB: -15% +/- 10%; P = 0.039), with no

125 ging but valuable model to gain insight into CTL biology.

126 In this study, we investigated CTLs specific for Pol epitopes in the immunogens in trea

127 een protofilaments in vitro FtsZ lacking its CTL (DeltaCTL) shows a dramatically increased propensity

128 click chemistry, resulting in Cy5.5-labeled CTLs (Cy5.5-CTLs).

129 hydrophobic organic charge-transport layers (CTLs).

130 ochondrial function between the control leg (CTL) and the immobilized leg (IMB).

131 was investigated by charge transition level (CTL) calculations for Nitrogen group (N, P, As, Sb) and

132 sholds, termed the 'critical thermal limit' (CTL).

133 Critical thermal limits (CTLs) are established viability thresholds when studying

134 features a hypervariable C-terminal linker (CTL) and a conserved C-terminal peptide (CTP).

135 intrinsically disordered C-terminal linker (CTL), and a C-terminal conserved peptide (CTC).

136 ppearance of CMV-CTLs with low (CMV tet(low) CTLs) and high tetramer binding (CMV tet(high) CTLs) in

137 These TMPs inhibit cytotoxic T lymphocyte (CTL) activity both in vitro and in vivo, and thus promot

138 oss-presentation and cytotoxic T lymphocyte (CTL) activity.

139 blish optimal CD8(+) cytotoxic T lymphocyte (CTL) memory for pathogens like the influenza A viruses (

140 generation of CD8(+) cytotoxic T lymphocyte (CTL) memory.

141 on or HIV-1-specific cytotoxic T lymphocyte (CTL) pressure shape the provirus landscape, we performed

142 An effective cytotoxic T lymphocyte (CTL) response against intracellular pathogens is general

143 d suppression of the cytotoxic T lymphocyte (CTL) response.

144 ly functional CD8(+) cytotoxic T lymphocyte (CTL) responses against a broad range of epitopes will li

145 sensitivities due to cytotoxic T lymphocyte (CTL) selected differences in Gag sequence but similar co

146 plexes that redirect cytotoxic T lymphocyte (CTL) specificity and function in response to the clonoty

147 Cytotoxic T lymphocyte (CTL)-based cancer immunotherapies have shown great promi

148 Vaccines that induce cytotoxic T lymphocyte (CTL)-mediated immune responses constitute an important c

149 tuximab (from 2000), cytotoxic T-lymphocyte (CTL) therapy (available in 1999-2004 and from 2011), and

150 tuximab (from 2000), cytotoxic T-lymphocyte (CTL) therapy (available in 1999-2004 and from 2011), and

151 CD8(+) cytotoxic T lymphocytes (CTL) and natural killer cells are the main cytotoxic kil

152 gh CD8(+) antitumor cytotoxic T lymphocytes (CTL) are the preferred effectors of cancer immunotherapy

153 protein 1 (PD-1) on cytotoxic T lymphocytes (CTL) in colon cancer.

154 late that enhancing cytotoxic T lymphocytes (CTL) targeting conserved envelope (Env) regions can elim

155 the ratio of CD8(+) cytotoxic T lymphocytes (CTL) to CD68(+) macrophages both predict disease-specifi

156 hanisms employed by cytotoxic T lymphocytes (CTL) to control tumors will aid in the development of im

157 n and activation of cytotoxic T lymphocytes (CTLs) and CD103+ cross-presenting dendritic cells (DCs),

158 hile v2.2 generated cytotoxic T lymphocytes (CTLs) and cleared virus within 10 days.

159 ytes-including CD8+ cytotoxic T lymphocytes (CTLs) and natural killer cells-and regulated by Runt-rel

160 terfering cytolytic cytotoxic T lymphocytes (CTLs) and NK cell contacts with tumor cells.

161 e formation between cytotoxic T lymphocytes (CTLs) and the target cells they aim to destroy is accomp

162 Cytotoxic T lymphocytes (CTLs) are thought to arrive at target sites either via r

163 CD8(+) cytotoxic T lymphocytes (CTLs) eliminate virally infected cells through directed

164 lar imaging of CD8+ cytotoxic T lymphocytes (CTLs) in response to anti-PD-L1 therapy.

165 Cytotoxic T lymphocytes (CTLs) kill infected and cancerous cells.

166 CD8 cytotoxic T lymphocytes (CTLs) rely on rapid reorganization of the branched F-act

167 vaccine priming of cytotoxic T lymphocytes (CTLs) requires the activity of endogenous DCs, suggestin

168 curs from activated cytotoxic T lymphocytes (CTLs) where they have recently been reported to complex

169 Cytotoxic T lymphocytes (CTLs) with strong abilities to suppress HIV-1 replicatio

170 de BCR-ABL-specific cytotoxic T lymphocytes (CTLs), endowed with antileukemia activity, from Ph(+) AL

171 killing mediated by cytotoxic T lymphocytes (CTLs), we performed genome-wide CRISPR screens across a

172 specific binding to cytotoxic T lymphocytes (CTLs).

173 umors, they exclude cytotoxic T lymphocytes (CTLs).

174 to evade killing by cytotoxic T lymphocytes (CTLs).

175 Cytotoxic T-lymphocytes (CTLs) and natural killer cells (NKs) kill compromised ce

176 Endogenous cytotoxic T-lymphocytes (CTLs) may not be adequate because of cellular exhaustion

177 Killer T cells (cytotoxic T lymphocytes, CTLs) maintain immune homoeostasis by eliminating virus-

178 xample, Ptpn2, Socs1 and Adar1) in mediating CTL evasion, and show that the lipid-droplet-related gen

179 e for the BCR or circulating Ab in mediating CTL responses to B cell-derived exosomes was ruled out u

180 the helped vs. unhelped IAV-specific memory CTL phenotype, with the unhelped set showing a more "exh

181 -specific CTL memory, with "unhelped" memory CTL exhibiting intrinsic dysfunction.

182 In addition, helped memory CTLs express the effector program characteristic of help

183 ection and the protective function of memory CTLs following challenge with an intracellular bacterium

184 Moreover, we identify that unhelped memory CTLs exhibit defects in a variety of energetic pathways,

185 Primary murine CTLs coordinate their migration in a process reminiscent

186 We demonstrate in primary murine CTLs that the a3-subunit of the vacuolar-type (H(+))-ade

187 safeguard mitochondrial function in nascent CTLs.

188 Nevertheless, CTLs lacking centrioles did display substantially reduce

189 +/- SEM: -3.6% +/- 0.5%; P = 0.030) but not CTL with no difference between supplementation groups.

190 Our characterization of CTL function provides a biochemical handle for understan

191 However, the combination of CTL exhaustion and the ability of HIV-1 to rapidly estab

192 of cellular exhaustion and the evolution of CTL-resistant viruses.

193 Epitope peptides, as a format of CTL vaccines, are being tested preclinically and clinica

194 ed an activation-induced immunodeficiency of CTL activity in ARPC1B-deficient patients, which could e

195 tially alleviates TMP-mediated inhibition of CTL activity, suggesting that the immunomodulatory effec

196 Introduction of CTL therapy was associated with improved survival.

197 , we show that loss of ARPC1B led to loss of CTL cytotoxicity, with the defect arising at 2 different

198 e of these subsets led to a complete loss of CTL response.

199 rs and in tumors with a greater magnitude of CTL responses.

200 rameterized based on in vivo measurements of CTL infiltration and killing rates applied to EL4/EG7 tu

201 Here, we show that suppression of CTL killing by CD4(+)CD25(+)Foxp3(+) regulatory T cell (

202 scriptome signatures from these two types of CTL responses revealed uniquely expressed gene clusters

203 uses containing lethal mutations upstream of CTL epitopes can also be recognized by CTLs, potentially

204 g priming promotes memory differentiation of CTLs.

205 ay as a conserved mediator of the evasion of CTLs by cancer cells, and show that this pathway is requ

206 cancer cells to orchestrate their evasion of CTLs, and shows that discrete functional modules that co

207 hypotheses regarding the hypervariability of CTLs and compare FtsZs to other bacterial proteins with

208 membrane proteins at the plasma membrane of CTLs, as recycling via the retromer and WASH complexes w

209 n after adoptive transfer of a population of CTLs.

210 lines that were cultured in the presence of CTLs.

211 ficiency of the stochastic search process of CTLs in the ECM should strongly be influenced by a dynam

212 agreed that the low measured killing rate of CTLs in vivo was insufficient to cause tumor regression.

213 The resulting resistance of CTLs to perforin explains their ability to kill target c

214 rating azide (N(3)) groups on the surface of CTLs via metabolic glycoengineering.

215 Evidently, adoptive transfer of CTLs pre-cultured with TMPs from irradiated breast carci

216 ned a universal CAR-T cell platform based on CTLs engineered to bind a variety of broadly neutralizin

217 t CD4(+) T cell help is required for optimal CTL responses and the establishment of memory, when and

218 during priming, CD4(+) T cell help optimizes CTL memory by creating T(EM) cells with innate and help-

219 Tx and prompt escalation to rituximab and/or CTL is recommended.

220 In right MTLE patients, CTL hypometabolism was the strongest predictor of an unf

221 individual CG, whereas the number of CG per CTL was unaffected.

222 by enhancing the number of IFNgamma-positive CTLs.

223 tor program characteristic of helped primary CTLs upon recall with MHC class I-restricted antigens, l

224 nation model, both cDC1 and RPM cross-primed CTL efficiently but with distinct kinetics.

225 lymphoid tissue and aim to elicit protective CTL-mediated immunity.

226 to antiviral immunity by generating a rapid CTL defense force that contains the virus until cDC1-ind

227 ts in comparison with control mice receiving CTLs pre-cultured with TMPs from untreated tumor cells.

228 V-CTLs and 3 weeks of observation.RESULTSEBV-CTLs did not induce significant toxicities.

229 Ag-loaded monocytes induced robust CTL responses via Ag transfer to splenic CD8+ DCs in a m

230 microg/g) and equivalent volumes of saline (CTL) were injected respectively to C57BL/6 mice for 6 we

231 In our ABM, we also simulated CTL production of the cytokine IFNgamma in order to expl

232 Because a single CTL can kill multiple targets, degranulation must be tig

233 e induction and regulation of HIV-1-specific CTL immunity, which is greatly determined by the context

234 hway during MDC1 induction of HIV-1-specific CTL responses inhibited the priming, activation, and dif

235 cause controllers have strong HIV-1-specific CTL responses, had a smaller proportion of intact provir

236 the overall magnitude of memory HIV-specific CTL responses and reversed the exhausted memory phenotyp

237 nfection for the maintenance of IAV-specific CTL memory, with "unhelped" memory CTL exhibiting intrin

238 We further detected NS3-specific CTL activities as well as CD107a expression of effector

239 s as an adjuvant to induce a robust specific CTL response.

240 ccination site promoted the vaccine-specific CTL response by enhancing expansion, short-lived effecto

241 ction of MUP was dependent on virus-specific CTL as deletion of such cells aborted MUP production.

242 cleared following transfer of virus-specific CTL.

243 Our results show that (p190)BCR-ABL-specific CTLs are capable of controlling treatment-refractory Ph(

244 d HIV vaccine-induced subtype C Env-specific CTLs in a macaque subtype B simian-human immunodeficienc

245 d greater frequencies of neoantigen-specific CTLs than soluble vaccines and even 31-fold greater than

246 yses further confirmed that the Pol-specific CTLs could effectively suppress HIV-1 replication.

247 ains unknown whether the Pol region-specific CTLs are equally efficient.

248 es simultaneous generation of tumor-specific CTLs and curtailment of tumor immunosuppressive environm

249 Here we show that VGLL1-specific CTLs expanded from the blood of a PDAC patient could rec

250 re important, exosomes from IL-12-stimulated CTLs directly activated bystander naive CD8(+) T cells t

251 rol exosomes derived from antigen-stimulated CTLs did not.

252 In an adenoviral infection model, such CTL contained the early viral spread, whereas cDC1 induc

253 ishing feature of CD4+ T cells that survived CTL killing.

254 This work suggests that CTL selection does not significantly check clonal prolif

255 Although we recently demonstrated that CTLs specific for 5 Gag epitopes in the vaccine immunoge

256 Here, we report that CTLs achieve this via two protective properties of their

257 These results show that CTLs constantly lag epitope mutation, suggesting that pr

258 with good clinical outcome, suggesting that CTLs specific for these 6 Pol epitopes had a strong abil

259 The CTL/macrophage ratio was significantly different between

260 Although the CTL and the target cell are both exposed to perforin wit

261 a supports a compact heterodimer between the CTL domains.

262 dings on human cells, free ISG15 boosted the CTL response in vivo via NK cells in the absence of CD4(

263 Here, we describe a role for the CTL of Caulobacter crescentus FtsZ as an intrinsic regul

264 lonal stability and number of clones for the CTL response against an epitope are inversely associated

265 ver, free ISG15 is a potent adjuvant for the CTL response.

266 Accordingly, in full-length Bs-FtsZ, the CTL acts as a spacer that spatially separates the CTP st

267 ions, resolve three bottleneck issues in the CTL epitope presentation pathway: vaccine uptake, phagol

268 The joint contributions of the CTL and CTP make Bs-FtsZ, an enzyme that is only half as

269 stroy is accompanied by reorientation of the CTL centrosome to a position beneath the synaptic membra

270 ape may require coordinated direction of the CTL clonal repertoire to simultaneously block escape pat

271 newly recognized innate route to promote the CTL response.

272 hile we found that Pol peptides promoted the CTL epitope presentation; we also discovered Pol peptide

273 nment-responsive NP further strengthened the CTL epitope presentation and CTL responses.

274 reatments, but it was not different than the CTL diets fed at these CP levels.

275 We also find that the CTL weakens GTP binding while enhancing the catalytic ra

276 Our in vitro studies show that the CTL weakens the driving forces for forming single-strand

277 target cell membrane is disrupted, while the CTL is invariably spared.

278 Combination of the MIP signature with the CTL/macrophage ratio stratified patients into three risk

279 o demonstrates that without manipulating the CTLs mediated response extensively, it is difficult to t

280 cessarily due to cooperative behavior of the CTLs.

281 Subsequently, azide groups on the CTLs were chemically labeled with near infrared fluoresc

282 opulations could be reengaged to support the CTLs, converting a weak primary antitumor immune respons

283 These CTL-derived vesicles contain CTL proteins and exhibit ma

284 xn phosphorylation with saracatinib in these CTL clones also severely compromised their functional ac

285 These CTLs rapidly eliminate N-peptide-displaying cells and dr

286 Thus, CTLs recognising a cognate target can induce a localised

287 ncreased hemagglutination-inhibition titers, CTL activity, and earlier virus clearance after homologo

288 c resistance of reservoir-harboring cells to CTL killing.

289 itivity or the resistance of cancer cells to CTL-mediated toxicity.

290 mproved economic efficiency when compared to CTL diets.

291 tricular (A-V) block in ZO-1cKO comparing to CTL hearts.

292 the endogenous antiviral response but not to CTL memory generation.

293 ANOG and autophagy involved in resistance to CTL under hypoxia.

294 of CCR2 increased cancer cell sensitivity to CTLs and enabled the cancer cells to induce DC maturatio

295 Ca(2+) signalling in adoptively transferred CTLs enhances T cell activation and IFN-gamma production

296 hromycin (TUL; n = 24); or (3) no treatment (CTL; n = 21).

297 ered in AV nodal cells of the ZO-1cKO versus CTL.

298 VZV-specific cytotoxic T cell (VZV-CTL) and T follicular helper responses to ZVL did not co

299 age, but similar to other Th1 responses, VZV-CTL peak and baseline responses were independently corre

300 roviding a potential mechanism through which CTLs control cortical actin density.