ライフサイエンスコーパス: cytotoxic

1 (>100% survival of GBM when challenged with cytotoxics).

2 s such as cadmium and arsenic are inherently cytotoxic.

3 ally contain 2-24 monomeric subunits and are cytotoxic.

4 eric protein with the uncaging of a powerful cytotoxic.

5 required for the conversion of the atypical cytotoxic 1-deoxysphinganine (1-deoxySA, m18:0) to 1-deo

6 o cancer cells causes NK cells to lose their cytotoxic ability and promote metastatic outgrowth.

7 cking down the expression of HRI resulted in cytotoxic accumulation of overexpressed alpha-synuclein,

8 The ensuing cytotoxic accumulation of psychosine results in diffuse

9 C5; survivin) expression) is synergistically cytotoxic across multiple models of basal-like TNBC and

10 tracts and their in vitro anti-proliferative/cytotoxic activities.

11 Antibody-dependent cell-mediated cytotoxic activity against FRalpha is also associated wi

12 lls exhibit improved expansion and increased cytotoxic activity against multiple tumor cell lines whe

13 NVS-CECR2-1 exhibits cytotoxic activity against various human cancer cells, k

14 C) levels of CD8+ T cells and enhanced their cytotoxic activity in a lymphoma coculture system.

15 atory potential, CD4(+) T cells also acquire cytotoxic activity marked by granzyme B (GzmB) expressio

16 creasing PD-L1 protein levels to enhance the cytotoxic activity of CD8(+) T cells.

17 r decreases CCL5 expression and augments the cytotoxic activity of tissue-resident T and NK cells, wh

18 portantly, TIDC were required to license the cytotoxic activity of tumor CD8(+) T cells, and in their

19 ly validated that afatinib has the strongest cytotoxic activity on BT474 (IC50 = 55.5 nM, BRCA2 and T

20 ween IL-6 serum levels and the impairment of cytotoxic activity suggests the possibility that targeti

21 ells, where the drug is released and induces cytotoxic activity.

22 It has been shown that it holds a high cytotoxic activity.

23 high antioxidant activity with an ignorable cytotoxic activity.

24 ls of proinflammatory cytokine secretion and cytotoxic activity.

25 e toxic shock syndrome, an escalation of the cytotoxic adaptive immune response triggered upon the bi

26 are used as a food, we found that quinoin is cytotoxic against BJ-5ta (human fibroblasts) and HaCaT (

27 rformed structural studies and show that the cytotoxic agent 7A-O-demethoxy-amino-noscapine (7A-amino

28 ia in human cancers compared to the parental cytotoxic agent and the vehicle groups.

29 Our strategy, which entails targeting of a cytotoxic agent, through a covalent enzyme inhibitor tha

30 Drug conjugates are chemotherapeutic or cytotoxic agents covalently linked to targeting ligands

31 c drugs have been widely described as potent cytotoxic agents for cancer cells.

32 Mutational signatures analysis showed how cytotoxic agents introduce hundreds of unique mutations

33 In the presence of cytotoxic agents, colonies reduced their variance in gro

34 lity control system, leading to formation of cytotoxic aggregates.

35 ich potentially could overwhelm clearance of cytotoxic alphaSN species.

36 with insufficient delivery resulting in sub-cytotoxic amounts of radioactivity being delivered to th

37 ectors induced the production and release of cytotoxic amyloids from lung endothelium, including beta

38 neumonia elicits endothelial cell release of cytotoxic amyloids that can be recovered from the bronch

39 ompetent P aeruginosa infection produced non-cytotoxic amyloids with antimicrobial properties.

40 on photoabsorbance showed that PBS was least cytotoxic and an optimal control for this study.

41 These data indicate that the combination of cytotoxic and cytostatic agents could represent an impor

42 y multiple HLA regions, suggesting that both cytotoxic and helper T-cell responses are important.

43 nteraction is crucial for inducing effective cytotoxic and humoral responses against pathogens.

44 king accumulation of CD8 T cells with highly cytotoxic and proliferative states and no evidence of re

45 ELs), a heterogeneous T cell population with cytotoxic and regulatory properties, which can be acquir

46 drug conjugates (ADCs) exhibited significant cytotoxic and target-mediated selectivity on human cance

47 re tested on human fibroblasts: they are not cytotoxic and they do not activate cells in a pro-inflam

48 ipation of (223)Ra-induced antiproliferative/cytotoxic bystander effects in delayed growth of DTC xen

49 after stimulation and associated changes in cytotoxic capacity in virus-specific memory cells in det

50 Clarifying the requirements for maximal cytotoxic capacity is critical to understanding how vira

51 ndocytic recycling, suggesting APOL1 forms a cytotoxic cation channel in the parasite plasma membrane

52 Cytotoxic CD4 T cells are linked to cardiovascular morbi

53 indings are consistent with a model in which cytotoxic CD4 T cells contribute to CVD in HIV/CMV coinf

54 ands CD70 and OX40L, thereby inducing potent cytotoxic CD4(+) and CD8(+) T cell responses.

55 and mucosal HIV Gag-specific poly-functional/cytotoxic CD4(+) and CD8(+) T cells were detected with t

56 Surprisingly, we also find multiple cytotoxic CD4(+) T cell states that are clonally expande

57 approach for rapid production of autologous cytotoxic CD4(+) T cells against a wide range of endogen

58 chanisms underpinning the differentiation of cytotoxic CD4(+) T cells following immunotherapy.

59 Memory CD4 and cytotoxic CD8 T cells appeared early in islets, accompan

60 hil extracellular traps (NETs), and excludes cytotoxic CD8 T cells from tumors.

61 In chronic HIV infection, virus-specific cytotoxic CD8 T cells showed expression of checkpoint re

62 Cytotoxic CD8(+) T cells are key for immune protection a

63 Activation of cytotoxic CD8(+) T cells by cross-priming DC contributes

64 Cytotoxic CD8(+) T cells can effectively kill target cel

65 patients had fewer neutrophils, while their cytotoxic CD8(+) T cells were activated, reflected as hi

66 ting with an increase in the infiltration of cytotoxic CD8(+) T cells.

67 self-antigen from necrotic cardiac cells to cytotoxic CD8(+) T cells.

68 from breast cancer patients, also increases cytotoxic CD8(+) T cells.

69 on, likely because of dampened activation of cytotoxic CD8(+) T cells.

70 NAs significantly increase the population of cytotoxic CD8+ T cells and simultaneously decrease the p

71 PD1 effects appear to be largely mediated by cytotoxic CD8+ T cells in solid tumors, HRSCs frequently

72 hich inhibits infiltration of tumor-specific cytotoxic CD8+ T cells.

73 rtk inhibition was abrogated by depletion of cytotoxic CD8alpha T cells by using anti-CD8alpha mAb or

74 CD8+ T lymphocytes, granzyme B production by cytotoxic cells (cytotoxic T cells and natural killer ce

75 The oligomeric OTUB1 aggregates were highly cytotoxic, characteristic of many amyloid proteins.

76 We applied the PDXGEM to several cytotoxic chemotherapies as well as targeted therapy age

77 Here, we show that cytotoxic chemotherapies induce dynamic changes in the t

78 We hypothesized that cytotoxic chemotherapy administered within 35 days of a

79 Cytotoxic chemotherapy administration was not significan

80 ound here that exposure of TNBC cells to the cytotoxic chemotherapy drugs cisplatin and doxorubicin a

81 ogical malignancies who are hospitalized for cytotoxic chemotherapy in noncritical care units.

82 to identify evidence that cancer patients on cytotoxic chemotherapy or other anticancer treatment are

83 arcomas (STSs) are mesenchymal tumours where cytotoxic chemotherapy remains the primary approach for

84 281 (35%) patients had received cytotoxic chemotherapy within 4 weeks before testing pos

85 generally far better tolerated than classic cytotoxic chemotherapy, this treatment, too, may be acco

86 skeletal event and the time to first use of cytotoxic chemotherapy.

87 nations that achieve deep remissions without cytotoxic chemotherapy.

88 HNSCC where comorbidities prevent the use of cytotoxic chemotherapy.

89 s a targeted inhibitor rather than a broadly cytotoxic chemotherapy.

90 c and adult cerebral malaria with a stronger cytotoxic component in adults, supporting the developmen

91 herapeutic potential in combination with non-cytotoxic compounds is poorly understood.

92 Cytotoxic compounds that target the ER often exhibit sel

93 ionally, treatment of cells using moderately cytotoxic concentrations of pine WSPM, carvacrol, and ot

94 he context of high or low CD8(+) T cells and cytotoxic contents.

95 The data thus indicated that the cytotoxic/cytostatic action of BRB at 10-30 muM might be

96 murine EMP-derived NK cells, harbor a potent cytotoxic degranulation bias.

97 gnition, M1-specific T cells rapidly undergo cytotoxic degranulation, release granzyme B and proinfla

98 reased surface CD107a expression, indicating cytotoxic degranulation.

99 ls to 43, 41, or 39 degrees C (which was not cytotoxic) dramatically increased their killing by prote

100 The major molecular mode of action of the cytotoxic drug 5-fluorouracil (5-FU) is generally consid

101 en conjugated one of these nanobodies to the cytotoxic drug doxorubicin, and we show that the conjuga

102 ug-tolerant "persisters" (DTPs), can survive cytotoxic drug exposure despite lacking resistance-confe

103 r DNA targeting chemotherapeutics and reduce cytotoxic drug resistance.New generation antibiotics suc

104 ability of liposome particles containing the cytotoxic drug to cross the placenta.

105 se membrane permeability, enhancing cellular cytotoxic drug uptake in tumors.

106 based on the nonselective bioconjugation of cytotoxic drugs to lysine and cysteine residues.

107 rapy is currently shifting from broadly used cytotoxic drugs to patient-specific precision therapies.

108 rs that are sensitive to other p53-dependent cytotoxic drugs, also display increased sensitivity to X

109 o tumors, which then allow the use of highly cytotoxic drugs.

110 CM and LBG hydrolysates (1 mg/mL) have shown cytotoxic effect and reduced cell viability of Caco-2 ce

111 eration of Caco-2 cell lines, exhibiting non-cytotoxic effect for HIMEC non-malignant endothelial cel

112 tumor-to-kidney ratio and a more pronounced cytotoxic effect than did (177)Lu-DOTATOC.

113 creened 8 commercially available statins for cytotoxic effect, anti-TB activity, synergy with first-l

114 ion against viruses and tumors through their cytotoxic effector function.

115 lls gain cytolytic potential by upregulating cytotoxic effector proteins and IFN-gamma.

116 a type III secretion system (T3SS) to inject cytotoxic effector proteins into host cells.

117 When used as cytotoxic effectors, YT cells loaded with GrB attacked M

118 PP induced cytotoxic effects in CSCs and prevented metastasis forma

119 d aggregates have been demonstrated to exert cytotoxic effects in several diseases.

120 ylsulfanyl derivatives exerted submicromolar cytotoxic effects in vitro against a panel of cancer and

121 We hypothesized that in addition to the cytotoxic effects observed in cancer cells Amiodarone al

122 tantly, these compounds did not abrogate the cytotoxic effects of cisplatin on human cancer cells.

123 ere, we show that fibroblasts counteract the cytotoxic effects of HER2 kinase-targeted therapy in a s

124 have analyzed the impact of lidocaine on the cytotoxic effects of MMC in this setting.

125 Hence, the antimicrobial and cytotoxic effects of pomegranate husk were examined and

126 Melanoidins did not exert cytotoxic effects on Caco-2 and HUVEC cells (viability w

127 ypharmacological agents through multipronged cytotoxic effects on cancer cells.

128 the contribution of NKA inhibition to their cytotoxic effects on tumor cells.

129 inhibition of HuR had potent cytostatic and cytotoxic effects on tumor growth, and strongly suppress

130 e with acute stress, but persistent SGs have cytotoxic effects that are associated with several age-r

131 he amyloid aggregation process per se exerts cytotoxic effects through the interaction of amyloid int

132 e invasiveness of breast cancer with minimal cytotoxic effects, thus departing from the cytotoxicity-

133 wn that the treated melanin and LiP have low cytotoxic effects; however, the mediator of veratryl alc

134 ices for their effectiveness at removing the cytotoxic elements of each reagent, permitting accurate

135 tophagy reduced intracellular degradation of cytotoxic enzymes such as granzyme B, thus enhancing the

136 hemical stability studies of ETPs along with cytotoxic evaluation of our designed ETPs against A549,

137 identify and preselect CD8(+) T cells with a cytotoxic expression profile are lacking.

138 of the cellular prion protein (PrP(C)) into cytotoxic fibrils (PrP(Sc)).

139 Compound 1 was cytotoxic for both breast cancer cell lines and the majo

140 The extracts were not cytotoxic for PBMC in vitro up to 500 ug/ml, while immun

141 lls the role of CD56 (NCAM) in human NK cell cytotoxic function has not been defined.

142 anges that direct activation, proliferation, cytotoxic function, and epigenetic changes.

143 CD8(+) T cells do not rely solely on cytotoxic functions for significant HIV control.

144 CD29 also marked T cells with cytotoxic gene expression from different tissues in sing

145 nd anti-inflammatory (IC(50) = 72 ug/mL) and cytotoxic (GI(50) of 30-79 ug/mL) activities.

146 sion protein allows quantitative analyses of cytotoxic granule maturation, transport and fusion in vi

147 r of GNLY, but not other cell death-inducing cytotoxic granule proteins, strongly inhibits Lm in huma

148 as granzymes and perforin through fusion of cytotoxic granules (CG) at the target cell interface, th

149 on protein of granzyme B, a key component of cytotoxic granules involved in T cell-mediated target ce

150 particles led to a significant cell-mediated cytotoxic immune response with systemic effects.

151 chanism distinct from, and synergistic with, cytotoxic impairment.

152 ents for living organisms, but they are also cytotoxic in high concentrations.

153 Whereas this complex was highly cytotoxic in human cancer cells, it showed low toxicity

154 Results: (125)I-KX1 was highly cytotoxic in vitro across a panel of neuroblastoma cell

155 tion of TDP-43 localization and formation of cytotoxic inclusions.

156 Increased CD4- cytotoxic iNKT cells may contribute to immunopathology i

157 ulation of excess FA in cells is known to be cytotoxic, it is unknown if an increase in FA level migh

158 (CTL) and natural killer cells are the main cytotoxic killer cells of the human body to eliminate pa

159 es (T) and natural killer cells are the main cytotoxic killer cells of the human body to eliminate pa

160 establish CD2 signaling as key for mediating cytotoxic killing and granule polarization in freshly is

161 to that of cycloviolacin O2, one of the most cytotoxic known cyclotides.

162 ad leukoencephalopathy and one patient had a cytotoxic lesion of the corpus callosum.

163 everal pathways have evolved to repair these cytotoxic lesions by rejoining broken ends, among them t

164 i within the corpus callosum consistent with cytotoxic lesions of the corpus callosum (4.1%).

165 DNA double-strand breaks (DSBs) are highly cytotoxic lesions that can lead to chromosome rearrangem

166 GBS produce a pigmented, cytotoxic lipid, known as granadaene.

167 trategy used by L. monocytogenes to modulate cytotoxic LLO activity through the enzymatic activity of

168 Natural killer (NK) cells are cytotoxic lymphocytes of the innate immune system that a

169 In contrast, the cytotoxic marker expression by mucosal CD4(+) and CD8(+)

170 st virally infected cells using a variety of cytotoxic mechanisms, and patients who have defective NK

171 The enediynes are among the most cytotoxic molecules known, and their use as anticancer d

172 ple production of cytokines, chemokines, and cytotoxic molecules.

173 s with severe disease express high levels of cytotoxic molecules.

174 tokines, and that IFN-gamma(+) cells produce cytotoxic molecules.

175 respectively) and a substrate with the caged cytotoxic (monomethyl auristatin E: MMAE; a high-affinit

176 We detected transfer of cytotoxic multiprotein complexes, called supramolecular

177 sity, but they are often cationic and can be cytotoxic, nephrotoxic and/or ototoxic, which has limite

178 entify an extra-embryonic origin of potently cytotoxic NK cells, suggesting that ontogenic origin is

179 clinical studies of crolibulin combined with cytotoxic or immune-oncology agents.

180 ing capabilities of an antibody to deliver a cytotoxic payload to specific cell types.

181 ation of both hemiasterlin and taltobulin as cytotoxic payloads in antibody-drug conjugates (ADCs).

182 feration stimulating peptide (IDALNENK), and cytotoxic peptide (LIVTQTMK).

183 The first syntheses of the cytotoxic peptides lipovelutibols B and D are described.

184 The vaccine-induced T cells had a cytotoxic phenotype and were capable of trafficking to t

185 Notably, CD29(+) T cells maintained the cytotoxic phenotype during cell culture, suggesting a st

186 ify CMV coinfection as a major driver of the cytotoxic phenotype, characterized by elevated CD57 expr

187 IL-15 promotes the cytotoxic phenotype, elevates CX3CR1 expression, and enh

188 cells, of monofunctional, polyfunctional and cytotoxic phenotypes, were also induced.

189 ncodes proteins involved in synthesis of the cytotoxic polyketide malleilactone; trimethoprim does so

190 ental to cells due to its high mutagenic and cytotoxic potential and is repaired by the alkyltransfer

191 abel treatment with tocilizumab restored the cytotoxic potential of NK cells.CONCLUSIONThe associatio

192 ance cellular adhesiveness to maintain their cytotoxic potential.

193 levels commonly needed for actuation can be cytotoxic, precluding long-term experiments.

194 nical mechanisms unrelated to the previously cytotoxic properties attributed to HDAC inhibitors.

195 rus (r2Reovirus) with enhanced infective and cytotoxic properties in TNBC cells.

196 uman NK cells rely largely on five different cytotoxic proteases, called granzymes (A/B/H/K/M).

197 ese changes are followed by reduction of the cytotoxic protein levels and increased skeletal muscle c

198 CTLs release cytotoxic proteins such as granzymes and perforin throug

199 therapies that react with the LIP to produce cytotoxic radical species (in some cases also releasing

200 reating hypoxic tumors since lower levels of cytotoxic reactive oxygen species (ROS) are generated in

201 ctivated DC with increased proliferation and cytotoxic response (CD107a and IFN-gamma-producing CD3+

202 reduced tumor sizes in vivo and enhanced the cytotoxic response to ionizing radiation.

203 bacterial infections because of their rapid cytotoxic responses at mucosal services to a widely cons

204 Here we discuss how cytoprotective and cytotoxic signaling modules activated by radiation in sp

205 RB1 (CD161) and displayed an innate-like low cytotoxic state, with low clonal expansion, unlike the c

206 stem cell (Lgr5(+)ISC) resilience following cytotoxic stresses is central to this repair stage.

207 ve bacteria functions in the defense against cytotoxic substances, such as antibiotics.

208 se tumors were sensitive to treatment with a cytotoxic substrate of NAT2 (6-(4-aminophenyl)-N-(3,4,5-

209 + T cells that persists despite HIV-specific cytotoxic T cell (CTL) responses.

210 actions were significantly lower, while CD8+ cytotoxic T cell fractions were significantly higher, co

211 viral interference with the ultimate step in cytotoxic T cell function, the death of infected cells.

212 in EOC tissue and inversely correlated with cytotoxic T cell infiltration, suggesting that HE4 may c

213 40 pathway in the mouse cancer model boosted cytotoxic T cell infiltration.

214 Ex vivo examination of cytotoxic T cell responses to the entire HIV-1 proteome

215 tial role in the elicitation of antibody and cytotoxic T cell responses.

216 integral to human T helper type 1 (Th1) and cytotoxic T cell responses.

217 ellular innate immune responses and adaptive cytotoxic T cell responses.

218 INCR1 knockdown sensitizes tumor cells to cytotoxic T cell-mediated killing, improving CAR T cell

219 get N for cytosolic degradation and generate cytotoxic T cells (CTLs) against N peptide.

220 tory signaling that enhances the activity of cytotoxic T cells (CTLs) could identify potential target

221 L) sensitized cells to lysis by EBV-specific cytotoxic T cells (EBV-CTLs).

222 y collagen were less efficient at attracting cytotoxic T cells and capable of inhibiting T cell proli

223 tumors had significantly few CD8(+)/PD-1(+) cytotoxic T cells and more CD25(+)/FOXP3(+) regulatory T

224 s, granzyme B production by cytotoxic cells (cytotoxic T cells and natural killer cells), and interle

225 ll lines to differentiation antigen-specific cytotoxic T cells and observe strong enrichment of a pre

226 Cytotoxic T cells clear virus-infected host cells and co

227 D-1 and interleukin-10 (IL-10) expression by cytotoxic T cells in H5N1 (2:6)-infected mice, suggestin

228 ty to activate both CD4(+) helper and CD8(+) cytotoxic T cells in response to necrotic cells and may

229 iferation and activation of insulin-reactive cytotoxic T cells in vitro.

230 o an immunoresponsive one by recruiting CD8+ cytotoxic T cells into tumor beds.

231 Restoring the levels and activity of cytotoxic T cells is a promising anticancer strategy; bu

232 Cytotoxic T cells play a key role in adaptive immunity b

233 Empowering the ability of cytotoxic T cells to kill tumor cells or the reframing o

234 olecules are designed to engage and activate cytotoxic T cells to kill tumor cells.

235 unotherapies act by enhancing the ability of cytotoxic T cells to kill tumor cells.

236 -DQ8 have a crucial role in the licensing of cytotoxic T cells to mediate intestinal epithelial cell

237 Activation of intraepithelial cytotoxic T cells with IL15 or IL21 induced separate sig

238 ycle progression, suppressed infiltration of cytotoxic T cells, and accelerated SCLC.

239 s formed in WNT5A knockout mice had elevated cytotoxic T cells, increased M1 macrophages, and decreas

240 d activated T cells, naive helper T (Th) and cytotoxic T cells, loss of CD56bright regulatory NK cell

241 lectively and its effects on intraepithelial cytotoxic T cells.

242 atively activated intestinal intraepithelial cytotoxic T cells.

243 al clearance is mediated by the functions of cytotoxic T cells.

244 electively bind peptides for presentation to cytotoxic T cells.

245 dedifferentiated cell state upon exposure to cytotoxic T cells.

246 These TMPs inhibit cytotoxic T lymphocyte (CTL) activity both in vitro and

247 s, tissue remodeling, and suppression of the cytotoxic T lymphocyte (CTL) response.

248 programmed cell death 1 ligand 1 (PD-L1) and cytotoxic T lymphocyte antigen 4 (CTLA-4) immune checkpo

249 Despite administration of cytotoxic T lymphocyte antigen 4 (CTLA-4) immunoglobulin

250 ntibodies targeting the checkpoint molecules cytotoxic T lymphocyte antigen 4 (CTLA4), programmed cel

251 the new mouse line is an ideal tool to study cytotoxic T lymphocyte biology and to optimize personali

252 D-1), programmed death ligand 1 (PD-L1), and cytotoxic T lymphocyte-associated protein 4 (CTLA-4) for

253 s programmed cell death protein 1 (PD-1) and cytotoxic T lymphocyte-associated protein 4 (CTLA-4), wh

254 1:programmed death ligand 1 (PD-1:PD-L1) and cytotoxic T lymphocyte-associated protein 4 (CTLA-4):B7-

255 mmune checkpoint inhibitors (ICIs) targeting cytotoxic T lymphocyte-associated protein-4 (CTLA-4) and

256 CD8(+) cytotoxic T lymphocytes (CTL) and natural killer cells a

257 ased gene signature, and the ratio of CD8(+) cytotoxic T lymphocytes (CTL) to CD68(+) macrophages bot

258 ol: increased infiltration and activation of cytotoxic T lymphocytes (CTLs) and CD103+ cross-presenti

259 rved in cytolytic lymphocytes-including CD8+ cytotoxic T lymphocytes (CTLs) and natural killer cells-

260 Immunological synapse formation between cytotoxic T lymphocytes (CTLs) and the target cells they

261 abody) for in vivo molecular imaging of CD8+ cytotoxic T lymphocytes (CTLs) in response to anti-PD-L1

262 of these proteins also occurs from activated cytotoxic T lymphocytes (CTLs) where they have recently

263 le cancer cells to evade killing mediated by cytotoxic T lymphocytes (CTLs), we performed genome-wide

264 ass I (MHC-I) expression to evade killing by cytotoxic T lymphocytes (CTLs).

265 ave also been investigated in detail; CD4(+) cytotoxic T lymphocytes (suspected of promoting disease)

266 Cytotoxic T lymphocytes (T) and natural killer cells are

267 vertebrate immune system and is secreted by cytotoxic T lymphocytes and natural killer cells to help

268 Close proximity between cytotoxic T lymphocytes and tumour cells is required for

269 od to reveal that sorting the most migratory cytotoxic T lymphocytes yields a pool of cells with enha

270 ckpoint therapy that revives tumour-reactive cytotoxic T lymphocytes, are effective in some patients(

271 1 upregulation protects them from killing by cytotoxic T lymphocytes, yet dampens the antitumor respo

272 and increased activation of antigen-specific cytotoxic T lymphocytes.

273 important for activation and persistence of cytotoxic T lymphocytes.

274 d engagement with their cognate receptors on cytotoxic T lymphocytes.

275 MARCO-expressing TAMs blocked cytotoxic T-cell and NK-cell activation, inhibiting thei

276 nt cohorts revealed strong associations with cytotoxic T-cell dysfunction and exclusion, respectively

277 gocytic engulfment and force dynamics in the cytotoxic T-cell immunological synapse.

278 onal signature that correlated with enhanced cytotoxic T-cell response in human solid tumors.

279 conditions of tumour cells induced systemic cytotoxic T-cell responses and immunological memory asso

280 s II region only, implying the importance of cytotoxic T-cell responses for the former and CD4(+) T-c

281 BNZ-2 might be used to prevent cytotoxic T-cell-mediated tissue damage in complex immun

282 First, ovalbumin (OVA) antigen-specific cytotoxic T-cells (CTLs) were incubated with N-azidoacet

283 e highest CD68 expression and associate with cytotoxic T-cells.

284 e assessed age-specific effects of CTLA4-Ig (cytotoxic T-lymphocyte antigen 4-Ig), a fusion protein b

285 tors, programmed death receptor-1 (PD-1) and cytotoxic T-lymphocyte antigen-4 (CTLA-4), respectively,

286 y ZMYND8 causes breast cancer cells to evade cytotoxic T-lymphocyte surveillance, which leads to tumo

287 and 1% preservative-free lidocaine were more cytotoxic than MMC and PBS (P < 0.01 for all).

288 ost hoc comparisons showed that MMC was more cytotoxic than PBS (P < 0.001).

289 ne at the reducing sugar prove that are more cytotoxic than their nonmethylated counterparts.

290 reatment for neuroblastoma than conventional cytotoxic therapies.

291 uM) and further restored the effect of a non-cytotoxic TMZ dose (10 muM).

292 tment successfully augmented the effect of a cytotoxic TMZ dose (50 muM) and further restored the eff

293 widespread reactivity, dienone compounds are cytotoxic to apoptosis-resistant tumor cells and show ac

294 e chemical properties of lanthanum making it cytotoxic to cancers, and able to enhance existing anti-

295 This inhibitor was mitochondria toxic and cytotoxic to colorectal cancer cells, but not to normal

296 Statins have been proven to be cytotoxic to human cholangiocarcinoma cells by inhibitin

297 ional systemic therapies, which are directly cytotoxic to tumour cells, cancer immunotherapy relies o

298 Peptide 4, now termed CHAT, was non-cytotoxic, traversed the plasma membrane of breast and p

299 tem-like properties and ability to resist to cytotoxic treatments.

300 : the nitroreductase/nitrofuran system and a cytotoxic variant of the M2 ion channel.