ライフサイエンスコーパス: CTL

1 CTL escape mutations restricted by protective HLA class

2 CTL expressing low-affinity TCR may be effective against

3 CTL responses to Ag-loaded exosomes were dependent on ho

4 CTL responses to the transgene product remain an active

5 CTL responses were tested against naturally HPV-infected

6 CTLs are serial killers that kill multiple target cells

7 s, the impact of programmed death -1 (PD-1), CTL-associated protein 4 (CTLA4), and T cell Ig and muci

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

9 A/StII) to assess their efficacy to induce a CTL response.

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

11 infection and that stronger selection across CTL epitopes is associated with favourable clinical outc

12 The absence of ITK both affected CTL expansion and delayed the expression of cytolytic ef

13 urdens was achieved by high- or low-affinity CTL.

14 e., the number of target cells killed by all CTLs) is well described by the previously derived double

15 IL-21 promotes B cell and CTL responses in vivo, conferring IL-21 with a role in b

16 y highlights the role of HIV replication and CTL control in reservoir accumulation in sanctuary sites

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

18 e CTLs also inhibited MTOC translocation and CTL-mediated killing.

19 memory cells (TRM cells), such as CD103, and CTLs from CD103(hi) tumors displayed features of enhance

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

21 as assessed under conditions where antitumor CTL expressed TCR of varying affinity for OVA.

22 Adoptive T cell therapy (ACT) with antitumor CTL is a promising and tailored treatment against cancer

23 We assessed CTL functionality by analysing selection in CTL-targeted

24 ly occurring HLA-B57- and HLA-B27-associated CTL escape mutations T242N and R264K resulted in delayed

25 demonstrate that dominant HLA-B27-associated CTL escape mutations within HIV-1 capsid lead to enhance

26 ed that HIV-1 downregulates HLA-A/B to avoid CTL recognition while leaving HLA-C unaltered in order t

27 mor burdens was unsuccessful, accompanied by CTL deletion and functional impairment.

28 effect was independent of that conferred by CTL density.

29 e-regulatory genes, essentially triggered by CTL-derived IFNgamma and augmented by TNFalpha.

30 n, and the replacement of wild-type virus by CTL escape mutants within the latent reservoir.

31 ed pore formation by perforin and killing by CTLs.

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

33 ction and morphology of exosomes secreted by CTLs can be influenced by the type of stimulation CTLs r

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

35 CD4 + CTL killing was also detected in FV-infected granzyme B

36 es CD4 Th cells, as well as cross-primes CD8 CTL responses.

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

38 Vaccine strategies to enhance CD8(+) CTL responses remain a current challenge because they sh

39 CD8(+) CTLs protect against parasite infections in mice primari

40 Pdcd1 (encodes PD-1) transcription in CD8(+) CTLs.

41 e patients have defective function of CD8(+) CTLs.

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

43 C virus (HCV) infection, cytotoxic T cells (CTL) are pivotal, but persistence of activated T cells m

44 elanocyte lines to cytotoxic CD8(+) T cells (CTL) using flow cytometry and gene expression analyses.

45 ides recognized by CD8(+) cytolytic T cells (CTL).

46 otein phosphorylations in cytotoxic T cells (CTL).

47 cy of T-helper/memory and cytotoxic T cells (CTLs) in peripheral blood mononuclear cells (PBMCs).

48 rast, the transfer of cytotoxic CD8 T cells (CTLs) led to both T-cell infiltration and specific destr

49 To kill multiple target cells, CTLs use endocytosis of membrane components of cytotoxic

50 et of LITRs on the surface of catfish clonal CTLs.

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

52 cted peripheral blood mononuclear cells, CMV-CTLs induced significantly less severe cutaneous GvH tis

53 une reconstitution of CMV-specific CTLs (CMV-CTLs) is essential for virus control.

54 Patients with dual CMV-CTLs had more CMV tet(high) than tet(low) CTLs.

55 Finally, dual CMV-CTLs were not associated with CMV antigenemia.

56 differentially tetramer binding ("dual") CMV-CTLs was unclear.

57 orting the safe use of in vitro expanded CMV-CTLs as an antiviral therapy in transplant patients with

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

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

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

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

62 measure R1 in 40 MDD and 40 healthy control (CTL) participants.

63 Well-coupled CTL myocytes are effectively voltage-clamped during Ca w

64 ansfer of WT but not BLT1(-/-) or CXCR3(-/-) CTLs significantly reduced tumor growth in Rag2(-/-) mic

65 n Spag6KO mice was associated with defective CTL functions and impaired humoral immunity as indicated

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

67 Furthermore, RAB27a-deficient CTLs, which do not secrete cytotoxic granules, failed to

68 is study, the consequences of well-described CTL-associated p24 Gag sequence mutations for HIV-1 caps

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

70 The number of distinct CTL clones targeting each epitope is proposed to be an i

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

72 tion, whereas a lack of IL-21R downregulates CTL responses that would otherwise limit B cell hyperact

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

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

75 ing to tell a different story, in which each CTL killed only 2-16 targets a day, and several CTLs per

76 sulted in transient activation of endogenous CTL in transgenic mice.

77 In summary, 3pRNA is a superior adjuvant for CTL activation and might be useful to facilitate antivir

78 g-specific donor CD8 T cells is critical for CTL effector maturation, whereas a lack of IL-21R downre

79 vate HS CD4(+) T cells that are required for CTL activation/maintenance and B cell maturation.

80 we derived a general functional response for CTL killing while considering that CTLs form stable syna

81 plication observed despite viral escape from CTL responses.

82 ct of coappearing CMV tet(low) and tet(high) CTLs after allogeneic SCT.

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

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

85 However, CMV tet(high) CTLs proliferated more in response to low CMV peptide co

86 lysis of isolated CMV tet(low) and tet(high) CTLs revealed their exclusive donor origin.

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

88 Isolated CMV tet(low) and tet(high) CTLs were equally sensitive to CMV peptides in IFN-gamma

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

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

91 ansion and rescued defective donor anti-host CTLs, resulting in host B cell elimination, decreased au

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

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

94 This could underlie the impaired CTL response in these neonates.

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

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

97 election were estimated for each gene and in CTL-restricted and non-restricted epitopes.

98 Conversely, in CTL hearts, gap junction inhibition (carbenoxolone) decr

99 e a critical role for both BLT1 and CXCR3 in CTL migration to tumors and thus may be targeted to enha

100 ealed that Tregs were critically involved in CTL tolerance.

101 alytic and binding activities of proteins in CTL exosomes.

102 All regions in CTL hearts exhibited faster calcein diffusion than in HF

103 immunosuppression had stronger selection in CTL-restricted vs. non-restricted epitopes in gag and ne

104 CTL functionality by analysing selection in CTL-targeted HIV-1 epitopes following perinatal infectio

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

106 Importantly, inhibiting CG endocytosis in CTLs results in a significant reduction of their cytotox

107 Depletion of p150(Glued) in CTLs also inhibited CTL-mediated lysis.

108 trisphosphate (PtdIns(3,4,5)P3) by mTORC1 in CTLs.

109 ed volumes, decreased vascularity, increased CTL infiltrate, and Nrp1-depleted BMDM adopted a more an

110 depletion did not alter the exosome-induced CTL response.

111 These data indicate that infant CTLs can exert selection pressure on gag and nef epitope

112 molecular fingerprint' of tumor-infiltrating CTLs and identify potentially new targets for immunother

113 anscriptomic profiling of tumor-infiltrating CTLs from treatment-naive patients with lung cancer to d

114 Infused CTLs persisted with frequencies up to 2.9% of CD8(+) T c

115 letion of p150(Glued) in CTLs also inhibited CTL-mediated lysis.

116 In the absence of PI2 (Ins2(-/-)), CTL in pancreatic lymph nodes (PLNs) were more activated

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

118 tributed to reduced infiltration of knockout CTLs into tumors.

119 not facilitate the infiltration of knockout CTLs to tumors.

120 cacy correlated with failure of the knockout CTLs to infiltrate into tumors upon anti-PD-1 treatment,

121 hydrophobic organic charge-transport layers (CTLs).

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

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

124 low CMV peptide concentrations than tet(low) CTLs.

125 MV-CTLs had more CMV tet(high) than tet(low) CTLs.

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

127 pse formed between a cytotoxic T lymphocyte (CTL) and an infected or transformed target cell is a phy

128 in increased CD8(+) cytotoxic T lymphocyte (CTL) function.

129 t induction site for cytotoxic T lymphocyte (CTL) immunity to airborne pathogens and intranasal vacci

130 tment did not impair cytotoxic T lymphocyte (CTL) recognition and killing of infected cells.

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

132 ve immunity, such as cytotoxic T lymphocyte (CTL) response, can result in promising antitumour effect

133 Cytotoxic T lymphocyte (CTL)-mediated killing involves the formation of a synaps

134 s (e.g. transmitted cytotoxic T- lymphocyte (CTL) escape mutations) or infant factors (e.g. reduced C

135 g strong CD8alpha(+) cytotoxic T-lymphocyte (CTL) responses remains lacking.

136 otent HIV-1-specific cytotoxic-T-lymphocyte (CTL) responses restricted by protective HLA alleles, but

137 ge, decreased CD8(+) cytotoxic T-lymphocyte (CTL) responses to novel pathogens and cancer is parallel

138 TERT-specific cytotoxic T lymphocytes (CTL) have been detected in the peripheral blood of B-cel

139 infection, although cytotoxic T lymphocytes (CTL) play a potentially critical role in eradication of

140 red by infiltrating cytotoxic T lymphocytes (CTL) without compromising tumor burden.

141 granule release by cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells.

142 any pathogens evade cytotoxic T lymphocytes (CTLs) by downregulating HLA molecules on infected cells,

143 ed on the idea that cytotoxic T lymphocytes (CTLs) directly recognize and respond to tumor-associated

144 ller (NK) cells and cytolytic T lymphocytes (CTLs) eliminate pathogen-infected cells by releasing cyt

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

146 -tumor responses of cytotoxic T lymphocytes (CTLs) have shown promise; however, clinical responses to

147 -1 from HIV-1-specific CD8(+) T lymphocytes (CTLs) is a major barrier for effective immune control.

148 -1 from HIV-1-specific CD8(+) T lymphocytes (CTLs) is a major barrier to effective immune control.

149 ng tumour-targeting cytotoxic T lymphocytes (CTLs) is one of the most effective immunotherapies again

150 Cytotoxic T lymphocytes (CTLs) kill target cells by the regulated release of cyto

151 mor-specific CD8(+) cytotoxic T lymphocytes (CTLs) play a critical role in an anti-tumor immune respo

152 irus (CMV)-specific cytotoxic T lymphocytes (CTLs) respond to allogeneic antigen stimulation and whet

153 Memory CD8(+)T lymphocytes (CTLs) specific for antigenic peptides derived from inter

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

155 alignant cells from cytotoxic T lymphocytes (CTLs).

156 d by HIV-1-specific cytotoxic T lymphocytes (CTLs).

157 cytotoxic T cells (cytotoxic T lymphocytes [CTLs]) against the HIV-1 Gag protein are associated with

158 T-cell (also called cytotoxic T lymphocytes, CTL) feedback activates the NLRP3 inflammasome in APCs i

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

160 -E-restricted autoaggressive effector memory CTLs specific for the immunodominant epitope 40-48 of my

161 elatively infrequent among IAV-primed memory CTLs.

162 of Pyk2 is spatially regulated in migrating CTL.

163 se disease was refractory to both monoclonal CTL and anti-CTLA4.

164 l calcium dependence of endocytosis in mouse CTLs on Flower, which mediates the calcium dependence of

165 own of NDE1 in Jurkat cells or primary mouse CTLs also inhibited MTOC translocation and CTL-mediated

166 Pyk2 function in murine CTL clones and activated ex vivo CD8(+) T cells was disr

167 cts of ITK deficiency on cytolysis in murine CTLs deficient in ITK, and both human and murine cells t

168 cells and OT-I TCR transgenic primary murine CTLs, we show that the dynein-binding proteins nuclear d

169 TCRbeta high-throughput sequencing in naive CTL of differently aged neonatal mice was performed, whi

170 decline in the number and function of naive CTL precursors (CTLp).

171 creased expansion of the endogenous neonatal CTL.

172 week of life and show that impaired neonatal CTL immunity results from an immature TCR repertoire, ra

173 individuals appears to have alternative, non-CTL mechanisms of viral control.

174 Local Ca waves depolarized Vm in HF but not CTL hearts, suggesting weaker gap junction coupling in H

175 The TCRalphabetas for HLA-B*3501-NP418 (+)CTLs varied among individuals and across IAV strains, in

176 2 is not absolutely required for adhesion of CTL to ICAM-1, but rather delays the initial adhesion.

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

178 rstanding of CTL identity and the control of CTL function by mTORC1.

179 to CTL migration by regulating detachment of CTL at the trailing edge, which could explain why Pyk2 i

180 thus may be targeted to enhance efficacy of CTL-based immunotherapies.

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

182 inical setting, they imply that the range of CTL and tumor-associated Ag combinations that may be eff

183 sponse they did not respond with a recall of CTL memory but, instead, with robust Ag-specific CTL tol

184 essed and promoted expression of a subset of CTL proteins (~10%).

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

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

187 nding should facilitate our understanding of CTL biology.

188 thus provides comprehensive understanding of CTL identity and the control of CTL function by mTORC1.

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

190 Tumors with a high density of CTLs showed enrichment for transcripts linked to tissue-

191 This response was independent of CTLs, natural killer or natural killer T cells.

192 rther aggravated upon repeated injections of CTLs.

193 prerequisite for efficient serial killing of CTLs and identify key events in this process.

194 eign peptides and can estimate the number of CTLs that can detect donor-matched transplants.

195 mune evasion casts new light on the roles of CTLs and NK cells in immune responses against HIV.

196 Interestingly, further stimulation of CTLs with IL-12 impacts exosome size and leads to select

197 n the effects of weak antigen stimulation on CTLs.

198 ss, because it takes typically more than one CTL to kill a target.

199 Cs results in either robust CTL tolerance or CTL memory, and this decision-making depends on the acti

200 cating scalable PSCs on all types of organic CTLs is reported.

201 d22 mice, yet the accumulation of pathogenic CTLs in the islets was significantly reduced in NOD-Idd2

202 ions, PRs, or stable disease, the persisting CTLs acquired phenotypic and functional characteristics

203 This expeditiously yielded polyclonal CTL lines uniformly expressing markers associated with a

204 by enhancing the number of IFNgamma-positive CTLs.

205 peptide and CpG (adjuvant) to elicit potent CTLs.

206 tion in the contraction phase of the primary CTL response they did not respond with a recall of CTL m

207 orks of protein phosphorylation that program CTL fate.

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

209 was presented by activated LCs, a recallable CTL memory response developed in transgenic mice.

210 c mechanism, the NS3-specific TCR-redirected CTLs were polyfunctional and inhibited HCV RNA replicati

211 e mutations) or infant factors (e.g. reduced CTL functional capacity) may explain this observation.

212 ght into actin-related mechanisms regulating CTL secretion that may facilitate serial killing during

213 and reduces the ability of HLA-C restricted CTLs to suppress viral replication in CD4+ cells in vitr

214 on by epidermal LCs results in either robust CTL tolerance or CTL memory, and this decision-making de

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

216 emia also occurs in the presence of selected CTL escape mutations.

217 killed only 2-16 targets a day, and several CTLs per target were needed to get the job done.

218 pport a variably dynamic process of shifting CTL clonality lagging in tandem with viral evolution and

219 gamma, TNFalpha, NF-kB signaling signatures, CTL-mediated apoptosis, mitochondrial dysfunction, and N

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

221 Analysis of NP(366-374)-specific CTL TCR repertoire revealed different Vbeta gene usage a

222 memory but, instead, with robust Ag-specific CTL tolerance.

223 ced IL-21-primed polyclonal antigen-specific CTL combined with CTLA4 blockade might boost antitumor e

224 fully functional, ongoing, antigen-specific CTL response may influence bystander CD8(+) T cells thro

225 tumor cell resistance to autologous-specific CTL and in vivo to the in situ recruitment of immune-sup

226 We studied insulin B-chain-specific CTL from different T-cell receptor transgenic mice (G9Ca

227 indings indicate that, although Gag-specific CTL may usually have greater anti-HIV efficacy than Env

228 peptides will prime different NP418-specific CTL sets.

229 OVA into Lp, elicited a similar OVA-specific CTL response to that observed with Lp/OVA/StII or vesicl

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

231 f CD103 integrin expressed on tumor-specific CTL clones promotes phosphorylation of Pxn and Pyk2 and

232 ting lymphocytes and CD103(+) tumor-specific CTL clones.

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

234 ologous or allogeneic (p190)BCR-ABL-specific CTLs.

235 itive feedback loop between antigen-specific CTLs and APC to amplify adaptive immunity.

236 ours to IFN-gamma-producing antigen-specific CTLs in vivo results in copy-number alterations (CNAs) a

237 , but the contribution from antigen-specific CTLs is not well understood.

238 Perforin from antigen-specific CTLs is required for NLRP3 inflammasome activation in AP

239 demonstrate that combining antigen-specific CTLs with CTLA-4 blockade is safe and produces durable c

240 Immune reconstitution of CMV-specific CTLs (CMV-CTLs) is essential for virus control.

241 Cytomegalovirus-specific CTLs isolated by the IFN-gamma secretion assay from HLA-

242 Cytomegalovirus-specific CTLs responded specifically to CMV-phosphoprotein 65 sti

243 Furthermore, when the insulin-specific CTLs developed in transgenic mice lacking their specific

244 velopment and activation of insulin-specific CTLs in the NOD mouse model of type 1 diabetes.

245 tients and Methods Autologous MART1-specific CTLs were generated by priming with peptide-pulsed dendr

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

247 This resulted in induction of specific CTLs producing cytokines and killing target cells in viv

248 TEIPP-specific CTLs recognize tumors defective in antigen presentation

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

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 can be influenced by the type of stimulation CTLs receive.

253 Evidence of stronger CTL selection was absent in infants with severe immunosu

254 HIV-1 is thought to subvert CTLs while preserving NK cell inhibition by Nef-mediated

255 D4(+) T cell activation status, and suppress CTL responses.

256 stimulates Treg differentiation, suppresses CTL activity and promotes HCC growth in an EGFR-dependen

257 Thus, tumor burden, rather than CTL affinity or avidity, appears to be the main determin

258 Taken together, these data demonstrate that CTL-driven escape mutations within p24 Gag restricted by

259 ponse for CTL killing while considering that CTLs form stable synapses (i.e., single-stage) and that

260 We found that CTLs secrete extracellular vesicles following antigen st

261 d cytotoxicity is one of the mechanisms that CTLs use to kill tumor cells.

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

263 The CTL proteome was dominated by metabolic regulators and g

264 of the interaction between the tumor and the CTL on the outcome of ACT against a mouse non-Hodgkin B

265 ants had lower levels of myelin than did the CTL participants at the whole-brain level and in the NAc

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

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

268 Moreover, the CTL affects the ability of the FtsZ curving protein FzlA

269 V-1 may require coordinated direction of the CTL clonal repertoire to simultaneously block escape pat

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

271 work that regulates approximately 10% of the CTL phosphoproteome, the production of phosphatidylinosi

272 model, we examined the TCR repertoire of the CTL response in neonatal and adult mice infected with in

273 always be implemented before infusion of the CTL.

274 ng rate exhibits a sigmoid dependence on the CTL density when killing is a multistage process, becaus

275 cal study of the effects of selection on the CTL recognition of TANs and completely foreign peptides

276 We conclude that the CTL of FtsZ influences polymer structure and dynamics bo

277 mice lacking their specific PI epitope, the CTLs demonstrated increased cytotoxicity and proliferati

278 cessarily due to cooperative behavior of the CTLs.

279 igmoid dependence of the killing rate on the CTLs during initial phases of killing may be indicative

280 Immunological analysis shows that while the CTLs expressing the NS5-specific TCR reduced HCV RNA rep

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

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

283 Thus, CTLs may change the landscape of HIV-1 proviruses by pre

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

285 in the processing and presentation of Ags to CTL, and insights into the mechanisms that govern peptid

286 contribution of CD4(+) and CD8(+) T cells to CTL and antitumor activity, respectively, was elucidated

287 Our results show that Pyk2 contributes to CTL migration by regulating detachment of CTL at the tra

288 nt role in immunity, yet its contribution to CTL responses has not been fully elucidated.

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

290 sustained anti-tumor activity of transferred CTL, as well as responses to nontargeted antigens, confi

291 Transferred CTLs trafficked to the pancreatic lymph node and prolife

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

293 ral years ago by the isolation of anti-tumor CTL that recognized spliced peptides, i.e. peptides comp

294 des, suggesting the possibility of universal CTL immunity in HLA-A*0201(+)individuals.

295 uent in HF (10.8% of myocytes, P<0.05 versus CTL).

296 weaker gap junction coupling in HF-AS versus CTL-AS myocytes.

297 Using an MHC II-restricted in vivo CTL assay we demonstrated that FV-specific CD4+ T cells

298 ulate HLA-C, possibly in response to whether CTLs or NK cells dominate immune pressure through HLA-C.

299 lity might be one of the mechanisms by which CTLs and IFN-gamma immunoedits tumours, altering their i

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

301 Cotransfer experiments suggested that WT CTLs do not facilitate the infiltration of knockout CTLs