ライフサイエンスコーパス: perforin

1 homing (CX3CR1) and cytotoxicity (NKG2D and perforin).

2 mice deficient in CD8 T-cells, IFN-gamma or perforin.

3 n conjunction with the pore-forming protein, perforin.

4 c hypertrophy and fibrosis, independently of perforin.

5 IS patients (p = 0.004) and were a source of perforin.

6 ), and express low levels of CD16, CD57, and perforin.

7 duced IFN-gamma, CD107(a/b), granzyme B, and perforin.

8 ctivity was not dependent on granzyme A/B or perforin.

9 vivo and begin to accumulate granzyme B and perforin.

10 ealed that CTL neurotoxicity was mediated by perforin.

11 ectively enhancing release of granzyme B and perforin.

12 al CD8(+) T cells expressed granzymes and/or perforin.

13 NK cells, as measured by the mobilization of perforin.

14 hosphatidylserine sequesters and inactivates perforin.

15 is of hkH37Rv-stimulated PBMC indicated that perforin 1 was the most significantly upregulated gene,

16 detected mRNAs for CD8(+) T-cell activation (Perforin 1, Granzyme B).

17 ipts for CD8, interferon (IFN)-gamma, CXCL9, Perforin 1, Granzyme B, and heat shock protein 60.

18 pression of cytotoxic (IFNgamma, granzyme B, perforin-1, Fas ligand) and apoptotic (cleaved caspase-3

19 n-gamma production and reduced expression of perforin-1.

20 signaling activities that 1) do not require perforin, 2) occur intracellularly, and 3) for which cel

21 The host-encoded Perforin-2 (encoded by the macrophage-expressed gene 1,

22 Perforin-2 (MPEG1) is a pore-forming, antibacterial prot

23 Perforin-2 (MPEG1) is an effector of the innate immune s

24 the membrane-associated pore-forming protein Perforin-2 (P2) is critical for LPS-induced endotoxic sh

25 In this study, we analyzed perforin-2 activity in the mouse placenta to determine w

26 findings suggest that the protective role of Perforin-2 against listeriosis is based on it limiting t

27 Here, it is shown that Perforin-2 also restricts the proliferation of the intra

28 er underscore the biological significance of Perforin-2 and elucidate critical molecular events that

29 itylation triggers a rapid redistribution of Perforin-2 and is essential for its bactericidal activit

30 if blocks ubiquitin dependent trafficking of Perforin-2 and thus, its bactericidal activity.

31 of 100 A pores in the bacterial surface with Perforin-2 cleavage products present in bacteria.

32 Perforin-2 constitutes a novel and apparently essential

33 Unexpectedly, inductive perforin-2 expression in decidual macrophages did not oc

34 In the placenta, inductive perforin-2 expression in decidual macrophages was coinci

35 ed in splenic macrophages in which inductive perforin-2 expression was observed in both high and mild

36 ning cullin-1 and betaTrCP monoubiquitylates Perforin-2 in response to pathogen associated molecular

37 Perforin-2 is a transmembrane protein of cytosolic vesic

38 Perforin-2 is also required for the bactericidal activit

39 We show that perforin-2 is critical for inhibiting Listeria monocytog

40 Perforin-2 is expressed constitutively in phagocytes and

41 Our results suggest that perforin-2 is part of a host response that is protective

42 Perforin-2 knockout mice are unable to control the syste

43 This cellular activity of Perforin-2 may derive from it regulating the acidificati

44 Perforin-2 mRNA is readily detectable in individual immu

45 e and others have shown that the host factor perforin-2 plays a central role in protecting mice and c

46 y in the mouse placenta to determine whether perforin-2 plays a similarly protective role.

47 Subsequently, Perforin-2 polymerizes and forms large clusters of 100 A

48 In vitro, Perforin-2 prevents the intracellular replication and pr

49 tively high level replicated equally well in Perforin-2(+/+)and Perforin-2(-/-)macrophages.

50 We go on to show in cultured Perforin-2(-/-)cells that the vacuole-to-cytosol transit

51 Unexpectedly, we found that in Perforin-2(-/-)macrophages,Listeria-containing vacuoles

52 eplicated equally well in Perforin-2(+/+)and Perforin-2(-/-)macrophages.

53 massive proliferation of L. monocytogenes in Perforin-2(-/-)mice leads to a rapid appearance of acute

54 Macrophage-expressed gene 1 (MPEG1/Perforin-2) is a perforin-like protein that functions wi

55 critical molecular events that culminate in Perforin-2-dependent killing of both intracellular and e

56 In contrast, Perforin-2-sufficient littermates clear the infection.

57 on is due to both maternal and fetal-encoded perforin-2.

58 ocytosis of specialized lysosomes containing perforin, a pore-forming protein, and granzymes, which a

59 ighly express the cytolytic granule proteins perforin-A, granzyme C (GzmC), and GzmA and surface rece

60 12.6% [7%-13.5%]; P < .05), and reduced CD8+ perforin activity (2.2% [0.1%-7%]; P < .05).

61 The ability to modulate perforin activity in vivo could be extremely useful, esp

62 force potentiates cytotoxicity by enhancing perforin activity.

63 patiotemporal colocalization of granzyme and perforin acts as an effective bimolecular filter to ensu

64 Many parasite effector proteins, including perforins, adhesins, and proteases, are extensively prot

65 ells also had impaired ability to re-express perforin after degranulation and reduced cytotoxic immun

66 When calcium is added to perforin already on the membrane, the QCM-D response cha

67 (IFN-gamma) alone or IFN-gamma together with perforin and (2) induction of proliferating cells that h

68 uding Fas/CD95 activation and the release of perforin and a group of lymphocyte granule serine protea

69 city, perforin MCF, CD107a MCF, and combined perforin and CD107a MCFs were 0.690, 0.971, 0.860, and 0

70 Perforin and CD107a tests are more sensitive and no less

71 We generated an AUC for combining perforin and CD107a tests by creating a logistic regress

72 ) NK cell subset had decreased expression of perforin and CD16 and a greater frequency of cells expre

73 st to the predicted closed ring observed for perforin and cholesterol-dependent cytolysins.

74 effector function due to impaired granzyme B/perforin and Fas/Fas ligand pathways and a phenotype of

75 ed two key effector molecules in CAR T cells-perforin and GM-CSF.

76 Cytotoxic T cells (Tc) use perforin and granzyme B (gzmB) to kill virus-infected ce

77 Experiments using inhibitors specific for perforin and granzyme B confirmed that CD8(+) T cell kil

78 4, and IL-21 cytokines; and NKT cell-derived perforin and granzyme B cytotoxins in promoting CD4(+) N

79 erferon-gamma, IL-4, and IL-21 cytokines and perforin and granzyme B cytotoxins, CD4(+) NKT cells fro

80 Stored PBMC were used for perforin and granzyme B ELISPOT and flow cytometry.

81 ptor PD-1, as well as the cytolytic proteins perforin and granzyme B in the infected mice.

82 lytic granules containing proteins including perforin and granzyme B, are secreted into the synaptic

83 granule exocytosis, involving the release of perforin and granzyme B, there is to date a lack of publ

84 KT cells potently promote atherosclerosis by perforin and granzyme B-dependent apoptosis that increas

85 a marked reduction in the cytolytic granules perforin and granzyme B.

86 ed the increased expression and secretion of perforin and granzyme B.

87 d expression of CD69 and cytotoxic molecules perforin and granzyme B; we also observed a correspondin

88 expression of cytotoxic effector molecules, perforin and granzyme beta, with reduced degranulation a

89 cal to preserve sufficient concentrations of perforin and granzyme for consistent pore formation and

90 and B cells, and the CD8(+) T cells produced perforin and granzyme.

91 toxicity by way of the cell killing proteins perforin and granzyme.

92 Since gene expression of perforin and granzymes A and B (GzmA and GzmB), cytolyti

93 ler cells and cytotoxic T-lymphocytes deploy perforin and granzymes to kill infected host cells.

94 on at the synapse and thereby the release of perforin and granzymes toward the target cell.

95 more cytotoxicity-associated genes including perforin and granzymes, and fewer genes associated with

96 with a target cell, followed by delivery of perforin and granzymes.

97 mune mouse Tc that selectively kill by using perforin and gzmB (gzmB(+)Tc) as effector cells and wild

98 it of RMA/B7H6 lymphoma-bearing mice through perforin and IFN-gamma effector mechanisms.

99 mediated both by NK and CD8+ T cells through perforin and IFN-gamma pathways.

100 cell contact reduced intracellular GrzB and perforin and increased surface-CD95L in NK cells over ti

101 creased expression of the effector molecules perforin and interferon-gamma with high expression of th

102 ed, circulating NK cells exhibited increased perforin and Ki67 expression levels and increased surfac

103 get cell tension augmented pore formation by perforin and killing by CTLs.

104 In contrast to homologous proteins such as perforin and the cholesterol-dependent cytolysins (CDCs)

105 y of CD8(+) T cells producing granzyme B and perforin and those expressing inhibitory receptors was h

106 within the synapse: high lipid order repels perforin and, in addition, exposed phosphatidylserine se

107 ct domains, a MACPF (membrane attack complex/PerForin) and a previously uncharacterized type of domai

108 argets and secreting a pore-forming protein (perforin) and pro-apoptotic serine proteases (granzymes)

109 ys and expressed messages for CD3gammadelta, perforin, and at least one of the CD4-like receptors as

110 mor necrosis factor-alpha, interferon-gamma, perforin, and CD107a expression) in 76 seropositive indi

111 ration, impaired expression of IFN-gamma and perforin, and diminished cytotoxicity against allogeneic

112 by increased CD69 expression and IFN-gamma, perforin, and granzyme B production, whereas NKT and mCD

113 F, expression of cytotoxic molecules (NKG2D, perforin, and granzyme B), and degranulation capacity of

114 cardiac NK cells secreted interferon gamma, perforin, and granzyme B, and expressed CD69, tumor necr

115 ed vesicles and SMAPs which contained TSP-1, perforin, and granzyme B.

116 iferated, and produced IFN-gamma, TNF-alpha, perforin, and granzymes upon in vitro stimulation, demon

117 +) T cells expressed low to medium levels of perforin, and subsets were activated and proliferating.

118 er RNA expression of inflammatory cytokines, perforin, and TRAIL by HSPC-NK cells.

119 mediated protective immunity, which involved perforin- and IFN-gamma-dependent effector mechanisms.

120 ceptible to NK cell-mediated fratricide in a perforin- and NKG2D-dependent manner.

121 d maternal T cells expressing granzyme B and perforin are enriched at the maternal-fetal interface (d

122 ponse changes significantly, indicating that perforin becomes membranolytic only after calcium bindin

123 We also found that cholesterol influences perforin binding and activity on intact cells and model

124 They constitutively express perforin but require preactivation to express granzyme B

125 y cytotoxic lymphocytes as soluble monomers, perforin can self-assemble into oligomeric pores of 10-2

126 tetramer frequency, granzyme B, granzyme K, perforin, CD107(a/b) cytotoxic degranulation, IFN-gamma,

127 NK cells with decreased expression of CD16, perforin, CD57, and impaired cytolytic function.

128 ncient branch of the Membrane Attack Complex-Perforin/Cholesterol-Dependent Cytolysin (MACPF/CDC) sup

129 Perforin-containing granules in NK cells from patients w

130 e ARM/HEAT domain led to a reduced number of perforin-containing granules, which were significantly i

131 Perforin contributed to both CD8+ and CD4+ CAR T cell cy

132 ess, the details of exactly how granzyme and perforin cooperate to induce target-cell death remain co

133 Given the established link between perforin deficiency and primary HLH, we investigated the

134 Surprisingly, combined perforin deficiency and transgenic IL-18 production caus

135 cess IL-18 promoted immunopathology, whereas perforin deficiency had no effect.

136 Depletion of AT1-ILCs and perforin deficiency resulted in alterations in the ratio

137 r CD8(+) T cells prevented toxicity, whereas perforin deficiency, GM-CSF deficiency, or modulation of

138 This was also true for perforin deficiency, which in the human causes a life-th

139 sens inflammation in a model of HLH in which perforin-deficient (Prf1 (-/-)) mice are infected with l

140 a model of primary (inherited) HLH in which perforin-deficient (Prf1(--)) mice are infected with lym

141 In the murine model of FHL, in which perforin-deficient (Prf1(-/-)) mice are infected with ly

142 latory effects were similar in wild-type and perforin-deficient animals.

143 Upon CAR-mediated in vitro activation, perforin-deficient CAR T cells produced higher amounts o

144 Thus, a murine model of perforin-deficient CAR T cells recapitulated late-onset

145 Following in vivo clearance of leukemia, perforin-deficient CAR T cells reexpanded, resulting in

146 was seen after engagement of Jurkat cells by perforin-deficient human cytotoxic lymphocytes.

147 Perforin-deficient mice (Prf1(null)) show early increase

148 rimental FHL mouse model in which disease in perforin-deficient mice is triggered by lymphocytic chor

149 er cytotoxic lymphocytes: it is abrogated in perforin-deficient mice or mice depleted of killer lymph

150 phocytic choriomeningitis virus infection of perforin-deficient mice, to study the activity and mecha

151 We found no primary Treg cell defects in perforin-deficient mice.

152 ctic protein) were reduced in mice receiving perforin-deficient NKT cells.

153 lapse of Treg cell numbers in LCMV-triggered perforin-deficient, but not wild-type, mice was accompan

154 tation of the biosensor technology to assess perforin-dependent and -independent induction of death p

155 Moreover, our results suggest that perforin-dependent cytotoxic mechanisms by CD8(+) T cell

156 erapeutic approach: exogenous IL-18 restored perforin-dependent cytotoxicity during infection by the

157 ls cleared hepatocyte replication niches via perforin-dependent cytotoxicity, whereas interferon-gamm

158 separate from the traditional role of GrB in perforin-dependent GrB-mediated apoptosis that could hav

159 s and follicular helper T cells (T(FH)) in a perforin-dependent manner during the first few days of i

160 infection rescued them from acute death in a perforin-dependent manner.

161 ells display a cytotoxic phenotype and use a perforin-dependent mechanism to control Ag-induced or T

162 In the current model of GrB activity, perforin determines whether the downstream actions of Gr

163 ylated extracellular membrane attack complex/perforin domain and the P2 domain independently associat

164 Finally, contrary to current thinking, perforin efficiently binds membranes in the absence of c

165 The resulting resistance of CTLs to perforin explains their ability to kill target cells in

166 The number of perforin-expressing cells in the lamina propria of acute

167 nd colleagues (2015) report that ablation of perforin-expressing dendritic cells induces T cell expan

168 These inversely correlated with perforin-expressing natural killer (NK) and CD3+ T cells

169 We observed a lower number of perforin-expressing NK cells in intensive care unit (ICU

170 in acute infection, with 2-fold increases in perforin expression and 3-fold increases in CD107a expre

171 acilitating treatment, but combining NK-cell perforin expression and CD107a upregulation tests can as

172 hocyte count and subtype, NK cell phenotype, perforin expression and degranulation, and natural or an

173 Perforin expression and the extent of degranulation have

174 ytotoxic program that includes granzymes and perforin expression at both early and late stages of inf

175 Pulmonary CD8 T cells showed lower perforin expression ex vivo compared with blood CD8 T ce

176 or ruxolitinib in vitro and in vivo restored perforin expression in CD56(dim) NK cells and partially

177 ing for granzyme biosensors was dependent on perforin expression in IL-2-activated NK effectors.

178 After seroconversion, perforin expression was downregulated in the lamina prop

179 erferon gamma production were observed; mean perforin expression was normal; and degranulation tests

180 ates with cytolytic capacity, as measured by perforin expression, a population not commonly present i

181 th increased IFN-gamma, ICOS, granzyme B and perforin expression.

182 bination resulted in an increase of NKs with perforin expression.

183 pients significantly correlated with reduced perforin expression.

184 asL, Granzyme A, Granzyme B, Granulysin, and Perforin following infection positively correlated with

185 Perforin from antigen-specific CTLs is required for NLRP

186 e spatiotemporal evolution of granzyme B and perforin from the time of their exocytosis to granzyme i

187 ablation of the cytolytic effector molecule perforin fully protected against vascular permeability a

188 d bone marrow stem cells in vivo by blocking perforin function.

189 cy and the levels of granzyme B, granzyme K, perforin, gamma interferon, tumor necrosis factor alpha,

190 T cells coexpressed the cytotoxic molecules perforin, granulysin, and granzyme B, which we termed po

191 rong bias toward a CX3CR1(+) Eomesodermin(+) perforin(+) granzyme B(+) CD45RA(+) CD4 CTL phenotype.

192 okine receptor (CCR)7(-) effector memory and perforin(+) granzyme B(+) cytotoxic cells, which express

193 of up to four functions (IFN-gamma(+)IL-2(+)Perforin(+)Granzyme B(+)).

194 8(+) T-cells that demonstrated an absence of Perforin, Granzyme and Zap-70, along with an enhanced ex

195 played greater cytolytic activity, secreting perforin, granzyme B, and Fas ligand when activated.

196 -)) CD8(+) T cells expressing high levels of perforin, granzyme B, and T-bet.

197 An increase in perforin, granzyme b, IFNgamma, TNFalpha and a loss of G

198 An increase in perforin, granzyme B, IFNgamma, TNFalpha, and a loss of

199 umours mainly by inducing cell death through perforin-granzyme and Fas-Fas ligand pathways(3,4).

200 Perforin/granzyme B content, degranulation (CD107a expre

201 Intracellular cytotoxic mediators (perforin/granzyme B), pro-inflammatory cytokines (IFNgam

202 Intracellular cytotoxic mediators (perforin/granzyme B), proinflammatory cytokines (IFNgamm

203 cytotoxic activity against target cells in a perforin/granzyme B-dependent manner.

204 Granule cytolytic perforin/granzyme C from this cell subsequently mediated

205 to control gammaHV-associated lymphoma, but perforin/granzyme is a more potent effector mechanism fo

206 tently infected mice use either IFN-gamma or perforin/granzyme to control gammaHV-associated lymphoma

207 tolytic degranulation pathway effectors (eg, perforin/granzyme).

208 ence of death receptor-induced apoptosis and perforin/granzyme-dependent cytotoxicity.

209 ages, but not against peritoneal cells, in a perforin/granzyme-dependent manner.

210 obilize intracellular Ca(2+) and to kill via perforin/granzyme.

211 bination of mediators of cytotoxicity, i.e., perforin, granzymes, and granulysin, and we called them

212 n(low) NK cells, with others by the CD56(dim)perforin(high) cytotoxic counterpart.

213 depends on PLP-CD8 elaborating IFN-gamma and perforin in a coordinated suppression program over time.

214 and primary HLH, we investigated the role of perforin in anti-CD19 CAR T cell efficacy and HLH-like t

215 with IL-21 in CD4 or CD107a, granzyme B and perforin in CD8 T cells following stimulation with HIV g

216 ut a role for NK cells as a single source of perforin in regulating glucose homeostasis.

217 e for the immune cytotoxic effector molecule perforin in regulating this process.

218 aired early apoptosis, suggesting a role for perforin in the regulation of T-cell turnover during HFD

219 Perforin-independent induction of apoptotic caspases was

220 eling and fibrosis through an extracellular, perforin-independent process.

221 Together, these results suggest a perforin-independent, extracellular role for GzmB in the

222 ls was largely intact in MDA5(-/-) mice, but perforin induction by natural killer cells and levels of

223 dentified series of benzenesulfonamide-based perforin inhibitors for their physicochemical and pharma

224 toxic proteases and the pore forming protein perforin into the synapse.

225 ation and elevated IFN-gamma, granzyme-B and perforin intragraft.

226 Because mutation in perforin is a common cause of FHL, we used an experiment

227 Perforin is a key effector protein in the vertebrate imm

228 Perforin is a key protein of the vertebrate immune syste

229 Perforin is an essential component in the cytotoxic lymp

230 The pore-forming protein perforin is essential for delivery of granzymes into the

231 e or interferon-gamma knock-out but not from perforin knock-out mice induced neuronal cell death in v

232 Adoptive CTL transfer from perforin knock-out or interferon-gamma knock-out mice in

233 Membrane attack complex/perforin-like (MACPF) proteins comprise the largest supe

234 The membrane attack complex (MAC)/perforin-like protein complement component 9 (C9) is the

235 age-expressed gene 1 (MPEG1/Perforin-2) is a perforin-like protein that functions within the phagolys

236 Egress requires secretion of a perforin-like protein, PfPLP2, from intracellular vesicl

237 were preferentially populated by CD56(bright)perforin(low) NK cells, with others by the CD56(dim)perf

238 nuscript, contains a membrane attack complex/perforin (MACPF) domain present in host immune molecules

239 S205F mutation in a membrane-attack-complex/perforin (MACPF)-domain protein, harbour altered endophy

240 Falpha, IFNgamma, interleukin 2, granzyme B, perforin, macrophage inflammatory protein 1beta, interle

241 AUCs for NK-cell cytotoxicity, perforin MCF, CD107a MCF, and combined perforin and CD10

242 Sensitivities of NK-cell function, perforin mean channel fluorescence (MCF), and CD107a MCF

243 ta2GPI-specific CD4(+) T lymphocytes express perforin-mediated and Fas/Fas ligand-mediated cytotoxici

244 ural killer (NK) cells-that share the direct perforin-mediated cytotoxic pathway on outcome after cer

245 mmatory role of NK cells is not dependent on perforin-mediated cytotoxicity.

246 t CD8 T cells initiate BBB breakdown through perforin-mediated disruption of tight junctions.

247 Development of OVA-AAD in perforin(-/-) mice suggested that the proinflammatory ro

248 The traditional view holds that perforin monomers assemble into pores in the target cell

249 f perforin on lipid membranes, and show that perforin monomers bind to the membrane in a cooperative

250 Without perforin, NK cells were unable to perform GrzB-mediated

251 uted to efficient tumor suppression, whereas perforin, NK cells, and CD4 T cells were not required.

252 Neither perforin nor GzmA was required; however, mice deficient

253 Regulatory effects of perforin on glucose tolerance are mechanistically linked

254 CM-D) to investigate binding and assembly of perforin on lipid membranes, and show that perforin mono

255 s mechanism to prevent rejection injury from perforin or granzyme B effectors and enhanced PI-9 or SP

256 Transfer of CD4(+) NKT cells deficient in perforin or granzyme B failed to augment atherosclerosis

257 sed by biallelic mutations in PRF1, encoding perforin, or UNC13D, STXBP2, STX11, RAB27A, LYST, and AP

258 r appeared gradually after a 90-min delay in perforin- or granzyme B-deficient CTLs.

259 es from cancer to autoimmunity, the granzyme-perforin pathway has been the subject of extensive inves

260 +) T cells induced pDC apoptosis through the perforin pathway.

261 ranzyme (Gzm) proteases and the pore-forming perforin (PFN)--into the infected cell.

262 Perforin (pfp)-mediated cytotoxicity is one of the princ

263 increased intra-tumoral NK cells expressing perforin plus IFN-gamma compared to untreated colon tumo

264 To elucidate the pathways of perforin pore assembly, we carried out real-time atomic

265 exertion across the synapse and the speed of perforin pore formation on the target cell, implying tha

266 from mRNA expression levels of granzyme and perforin, positively correlates with CD8+ T cell infiltr

267 the cytotoxic mediators granzyme B (GrB) and perforin (PRF) in CD8(+) T cells have yielded disparate

268 trolling most virus infections, primarily by perforin (PRF)- and granzyme B (GrB)-mediated apoptosis.

269 al killer (NK) cells to kill target cells by perforin (Prf)/granzyme (Gzm)-induced apoptosis causes s

270 of HLH pathology, we used the mouse model of perforin (Prf1)(KO) mice infected with lymphocytic chori

271 Furthermore, perforin production specifically by CD8 T cells was requ

272 developed predominant Th22-like and NK-like (perforin production) responses to M. tuberculosis infect

273 ns in HLH-associated genes, those coding for perforin, Rab27a, and syntaxin-11.

274 nd the inhibitory effect on Th1 and granzyme/perforin-related pathways.

275 Our data also indicate that CTLs coordinate perforin release and force exertion in space and time.

276 omesodermin, as well as the cytolytic enzyme perforin, required for the cytotoxic type 1 program.

277 ine producing T-cells towards an IFNgamma(+) perforin(+) response, suggesting increased cytotoxic fun

278 Perforin, secreted by immune cells, binds target membran

279 r model, a large amount of both granzyme and perforin still escape from the synapse.

280 tumor necrosis factor (TNF), granzyme B, and perforin than CD8+ T cells.

281 induced killer cells express, Granzyme B and Perforin that assault and kill other members of the AML

282 dies have examined the structure and role of perforin, the mechanics of pore assembly and granzyme de

283 Highest increase in the expression of perforin, the rate-limiting molecule for cytotoxic CD8(+

284 cytotoxic effector molecules granzyme B and perforin; their degranulation upon exposure to K562 cell

285 nce the function of the pore-forming protein perforin, thereby leading to more effective target cell

286 ase cytotoxic proteins such as granzymes and perforin through fusion of cytotoxic granules (CG) at th

287 8, CD56, CD103, PD1, CD30, ALK1, CD10, BCL6, perforin, TIA-1, Granzyme B and Epstein-Barr virus-encod

288 tural killer cells, which overwhelmingly use perforin to kill their targets.

289 uired to process precursors of granzymes and perforin to their mature form.

290 cally determine the relative contribution of perforin, TRAIL, and IFN-gamma-mediated pathways in prot

291 induced improved cell-cycle progression and perforin upregulation after autologous and emerging epit

292 ecting a lymphocyte cytotoxicity gene or the perforin variant A91V was observed in almost 50% of the

293 while secretion of the cytotoxicity molecule perforin was not enhanced.

294 Perforin was required for their invasion and cyst elimin

295 ory cytokine IFN-gamma, but not TNF-alpha or perforin, was essential to IL-15 SA-induced immunotoxici

296 In the absence of perforin, we show that GrB enzymatic activity still indu

297 IFN-gamma, IL-2, MIP-1beta, TNF, CD107a, and perforin) were identified by flow cytometry following au

298 tion involves the induction of granzymes and perforin, which are the main effector molecules expresse

299 nority of CD19(+) and IgA(+) cells expressed perforin with no difference between IBD and controls.

300 thin the calcium-binding regions, activating perforin with respect to membrane binding.

301 CTL and the target cell are both exposed to perforin within the synapse, only the target cell membra