ライフサイエンスコーパス: perforin

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

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

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

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

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

6 vivo and begin to accumulate granzyme B and perforin.

7 ealed that CTL neurotoxicity was mediated by perforin.

8 ectively enhancing release of granzyme B and perforin.

9 e detected and mainly attributed to secreted perforin.

10 t, CD8(+) T cells and the effector molecule, perforin.

11 and preserved levels of interferon-gamma and perforin.

12 e tumor site were dependent on IFN-gamma and perforin.

13 he lymphocyte-expressed pore-forming protein perforin.

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

15 c hypertrophy and fibrosis, independently of perforin.

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

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

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

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

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

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

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

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

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

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

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

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

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

29 Perforin-2 constitutes a novel and apparently essential

30 Interestingly, induction of perforin-2 expression in epithelial cells is blocked dur

31 Ectopic expression of perforin-2 in HeLa cells, however, does result in killin

32 Knockdown of perforin-2 in macrophages did not alter the invasion of

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

34 Perforin-2 is a transmembrane protein of cytosolic vesic

35 Perforin-2 is also required for the bactericidal activit

36 Perforin-2 is expressed constitutively in phagocytes and

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

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

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

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

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

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

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

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

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

46 hat identifies a novel host defense protein, perforin-2, that plays a significant role in the eradica

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

48 C. muridarum were all equally susceptible to perforin-2-mediated killing.

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

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

51 force potentiates cytotoxicity by enhancing perforin activity.

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

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

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

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

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

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

58 Perforin and CD107a tests are more sensitive and no less

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

60 ed volunteers, the expression of Granzyme A, Perforin and CD57 on influenza HLA A*02 M158-66 antigen

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

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

63 ion is dependent on CD8(+) T cells, involves perforin and gamma interferon (IFN-gamma), and is correl

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

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

66 of NK and cytotoxic T cell (CTL) expressing perforin and granzyme B and of CTL producing IFN-gamma w

67 4, and IL-21 cytokines; and NKT cell-derived perforin and granzyme B cytotoxins in promoting CD4(+) N

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

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

70 induction of cytolytic molecules, including perforin and granzyme B in response to IL-21.

71 D8, CTLA4, Foxp3, chemokine IP-10, cytotoxic perforin and granzyme B, and BKV VP1 mRNA were not diffe

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

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

74 vating receptor DNAM-1 and the lytic enzymes perforin and granzyme B.

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

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

77 Moreover, a significant increase in perforin and granzyme mRNA expression was observed in PB

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

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

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

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

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

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

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

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

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

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

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

89 Defects in perforin and related genes lead to a loss of normal immu

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

91 27 agonists promoted increased expression of perforin and the generation of short-lived memory cells,

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

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

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

95 tor alpha (TNF-alpha), interleukin-2 (IL-2), perforin, and CD107a.

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

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

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

99 , DNAX accessory molecule-1 (DNAM-1; CD226), perforin, and granzyme B.

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

101 g elevated levels of granzyme A, granzyme B, perforin, and IFN-gamma, we therefore evaluated carbopla

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

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

104 ent of vulnerable atherosclerotic plaques by perforin- and granzyme B-mediated apoptosis of macrophag

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

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

107 cing IFN-gamma, TNF-alpha, IL-17, IL-22, and perforin at the endpoint of more severe TB, but they pre

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

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

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

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

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

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

114 pleted macaques contained fewer IL-22(+) and perforin(+) cells despite the presence of IL-17(+) and I

115 Membrane attack complex/perforin/cholesterol-dependent cytolysin (MACPF/CDC) pro

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

117 Perforin-containing granules in NK cells from patients w

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

119 n hematopoietic cells through the release of perforin-containing lytic granules.

120 Perforin contains a membrane attack complex/perforin (MA

121 We used a murine model of HLH to examine how perforin controls immune activation, and we have defined

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

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

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

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

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

127 However, perforin-deficient alloreactive DLI induced significantl

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

129 down-regulated genes separated patients with perforin-deficient FHL from those with unidentified gene

130 ent, caspase 3/7 biosensor signal induced by perforin-deficient human CTLs was also detectable after

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

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

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

134 However, in contrast to perforin-deficient mice, the disease was transient, and

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

136 However, in contrast to perforin-deficient mice, which represent a model for FHL

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

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

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

140 tivity of both isolated perforin protein and perforin delivered in situ by natural killer cells was d

141 killer lymphocytes recognize infected cells, perforin delivers cytotoxic proteases (granzymes) into t

142 required several calcium flux events before perforin delivery.

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

144 ed whether the Plac8-dependent clearance was perforin-dependent by pharmacologically inhibiting iNOS

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

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

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

148 une regulation caused by mutations affecting perforin-dependent cytotoxicity.

149 This endogenous feedback loop involves perforin-dependent elimination of rare, antigen-presenti

150 r this protection, which is mediated through perforin-dependent lysis of infected cells and IFN-gamma

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

152 c function in vitro, reduced metastasis in a perforin-dependent manner, and enhanced NK cell expressi

153 dary effectors to kill infected targets in a perforin-dependent manner.

154 nd was lysed by chNKG2D-bearing T cells in a perforin-dependent manner.

155 ffector CTLs were capable of being killed by perforin-dependent mechanisms.

156 ofile, every target cell that was damaged by perforin died by apoptosis.

157 significantly, with a severity gradient from perforin (early onset) > Rab27a > syntaxin-11 (late onse

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

159 components of an miRNA network that controls perforin, eomesodermin, and IL-2Ralpha expression in dif

160 s, calcium influx into the lymphocyte led to perforin exocytosis and target cell permeabilization in

161 e has identified the role of granzyme B- and perforin-expressing CD4(+) T cells with cytotoxic potent

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

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

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

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

166 Perforin expression and the extent of degranulation have

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

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

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

170 cessful DC immunotherapy required IFN-gamma, perforin expression was dispensable.

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

172 stinct threshold of approximately 10% to 20% perforin expression with either mixed hematopoietic or C

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

174 pients significantly correlated with reduced perforin expression.

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

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

177 ectors exhibit multiple effector activities, perforin-, Fas ligand-, and TRAIL-mediated cytotoxicity,

178 Perforin from antigen-specific CTLs is required for NLRP

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

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

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

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

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

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

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

186 inducing CTL-associated cytotoxin responses (perforin, granzyme A, granzyme B).

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

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

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

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

191 Transfer of CD8(+) T cells deficient in perforin, granzyme B, or tumor necrosis factor alpha but

192 y immune recognition and killing through the perforin-granzyme pathway.

193 ic response, and there was evidence for both perforin/granzyme as well as Fas/Fas ligand-dependent pa

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

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

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

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

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

199 Conversely, the perforin/granzyme-mediated killing and IFN-gamma respons

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

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

202 The contribution of molecules such as perforin, IFN-gamma (IFNgamma), and particularly Fas lig

203 nation effects were dependent on host IL-12, perforin, IFN-gamma, natural killer, and/or T cells and

204 We conclude that the decreased level of perforin in lytic granules of LAMP1-deficient cells, com

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

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

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

208 Perforin-independent induction of apoptotic caspases was

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

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

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

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

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

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

215 Perforin is a key protein of the vertebrate immune syste

216 Perforin is an essential component in the cytotoxic lymp

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

218 In LAMP1 RNAi cells, more perforin is retained outside of lysosomal compartments i

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

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

221 In vivo, unexpectedly, clearance in perforin knockout mice was delayed to the end of week 7

222 knockout h3TA2 mice but not in TNF-alpha- or perforin-knockout h3TA2 mouse strains, confirming a cent

223 Two groups have shown that perforin-knockout mice were not compromised in their abi

224 dent by pharmacologically inhibiting iNOS in perforin-knockout mice.

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

226 The recently discovered role of a perforin-like protein (PLP1) for rapid host cell egress

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

228 tions for this sole Drosophila member of the perforin-like superfamily.

229 tissues were highly enriched in CD56(bright)perforin(low) cells, and the distribution of NK subsets

230 Besides solid tissues, CD56(bright)perforin(low) NK cells were also detected in seroma flui

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

232 Perforin contains a membrane attack complex/perforin (MACPF) domain and oligomerizes to form an aque

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

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

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

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

237 nation, with an additional contribution from perforin-mediated CD8(+) T cell apoptosis.

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

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

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

241 These findings demonstrate that perforin-mediated immunoregulation functions in trans an

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

243 D was studied using NK-deficient (NKD) mice, perforin(-/-) mice, and mice depleted of Ly49A/D/G(+) NK

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

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

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

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

248 Regulatory effects of perforin on glucose tolerance are mechanistically linked

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

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

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

252 by IFN-gamma without any involvement of the perforin or TRAIL-dependent pathways.

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

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

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

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

257 ent target cell rounding within 2 minutes of perforin permeabilization.

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

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

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

261 xhibit reduced tumor cytolysis and abrogated perforin polarization to the immune synapse.

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

263 ctive targets, we defined the time course of perforin pore formation in the context of the physiologi

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

265 that granzymes passively diffuse through the perforin pore into the cytoplasm of the target cell.

266 ytotoxic lymphocyte immune defense, in which perforin pores assemble on the target cell plasma membra

267 Here we demonstrate that perforin preferentially delivers cationic molecules whil

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

269 as coincident with a significant increase in perforin production by NK cells.

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

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

272 inhibit the lytic activity of both isolated perforin protein and perforin delivered in situ by natur

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

274 xpected to result in the complete absence of perforin, Rab27a, or syntaxin-11, we found that disease

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

276 cell death was correlated with the amount of perforin released by the NK cells.

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

278 this, the CTL membrane was not intrinsically perforin resistant, as intact CTLs presented as targets

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

280 aptic cleft, target cell permeabilization by perforin resulted in the rapid diffusion of extracellula

281 nt in vitro/in vivo results suggest that the perforin's contribution to bacterial clearance in vivo i

282 Perforin, secreted by immune cells, binds target membran

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

284 ght) CTLs expressed more granzyme B but less perforin than CD3(-)CD56(dim) NK cells.

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

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

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

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

289 pression of CD107a/LAMP-1 reduced binding of perforin to cells.

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 CD8(+) T-cell response but not with greater perforin upregulation.

293 In vitro we found that perforin was detrimental to iNOS-dependent CD4 T cell te

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

295 lloproteinase-1, fibronectin, granzyme B, or perforin were associated with graft failure.

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

297 duce cytolysis via releasing factors such as perforin, which permeabilizes target cells.

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

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

300 in the breach of the target cell membrane by perforin within 65-100 s.