ライフサイエンスコーパス: granzyme

1 egranulation pathway effectors (eg, perforin/granzyme).

2 ay of the cell killing proteins perforin and granzyme.

3 and the CD8(+) T cells produced perforin and granzyme.

4 t cell, followed by delivery of perforin and granzymes.

5 ells by producing cytokines, chemokines, and granzymes.

6 f lymphocyte granule serine proteases called granzymes.

7 an inhibitor, and an activity-based probe of Granzyme A (GrA) that can be used to follow functional G

8 ia RT-PCR and immunoblot, we discovered that granzyme A (GrmA), a serine protease not previously iden

9 a model tumor Ag, they selectively expressed granzyme A and directly lysed YAC-1 thymoma cells throug

10 eavable biosensors, we report development of granzyme A and granzyme K biosensors, for which no other

11 NA) than CD4(+) alphaE(-) cells (P < .0001); granzyme A and integrin alphaE protein were detected in

12 for autoimmunity, we examined the impact of granzyme A deficiency in the NOD mouse model of autoimmu

13 Granzyme A deficiency resulted in an increased incidence

14 autoimmune diabetes and an in vivo role for granzyme A in maintaining immune tolerance.

15 Granzyme A is a protease implicated in the degradation o

16 patients with UC expressed higher levels of granzyme A messenger RNA (GZMA mRNA) than CD4(+) alphaE(

17 17A, IFN-gamma, IL-10, IP-10, GM-CSF, sFasL, Granzyme A, Granzyme B, Granulysin, and Perforin followi

18 sulin in transgenic NOD mice was broken on a granzyme A-deficient background.

19 illi indirectly, via concentration-dependent granzyme A-driven apoptosis.

20 hat inversely correlated to the frequency of granzyme A-expressing NK cells.

21 Since gene expression of perforin and granzymes A and B (GzmA and GzmB), cytolytic proteins li

22 vels of expression of the cytolytic proteins granzymes A and B.

23 n five different cytotoxic proteases, called granzymes (A/B/H/K/M).

24 ctionally preprogrammed (e.g., IFN-gamma and granzymes-A/K), with properties of rapidly activatable i

25 llow interrogation of additional features of granzyme activity in live cells including localization,

26 important therapeutic target but additional granzyme and caspases inhibition is required for suffici

27 inly by inducing cell death through perforin-granzyme and Fas-Fas ligand pathways(3,4).

28 Nevertheless, the details of exactly how granzyme and perforin cooperate to induce target-cell de

29 ), calculated from mRNA expression levels of granzyme and perforin, positively correlates with CD8+ T

30 ls that demonstrated an absence of Perforin, Granzyme and Zap-70, along with an enhanced expression o

31 racheally into wild-type mice, IL-21 induced granzymes and augmented clearance of pulmonary MRSA but

32 inhibited a cytotoxic program that includes granzymes and perforin expression at both early and late

33 CTLs release cytotoxic proteins such as granzymes and perforin through fusion of cytotoxic granu

34 , which is required to process precursors of granzymes and perforin to their mature form.

35 llograft rejection involves the induction of granzymes and perforin, which are the main effector mole

36 e majority of total CD8(+) T cells expressed granzymes and/or perforin.

37 ere functionally programmed (e.g., IFNgamma, granzymes) and expressed low levels of terminal deoxynuc

38 ment, matrix metalloproteases, caspases, and granzymes, and carried by lymph, contribute significantl

39 city-associated genes including perforin and granzymes, and fewer genes associated with recirculation

40 f mediators of cytotoxicity, i.e., perforin, granzymes, and granulysin, and we called them polycytoto

41 me was dominated by metabolic regulators and granzymes, and mTORC1 selectively repressed and promoted

42 Overall, these data establish a granzyme- and granulysin-mediated innate immune mechanis

43 nterferon (IFN-gamma) and granzymes but that granzymes are not required for sucrase deficiency.

44 for restimulation of the cytotoxic mediators granzyme B (GrB) and perforin (PRF) in CD8(+) T cells ha

45 Granzyme B (GrB) initiates at least three distinct cell

46 Granzyme B (GrB) is an immune protease implicated in the

47 b9) results in the death of tumor cells in a granzyme B (GrB)-dependent manner.

48 infections, primarily by perforin (PRF)- and granzyme B (GrB)-mediated apoptosis.

49 s by releasing cytotoxic granules containing granzyme B (GrzB) or by engaging death receptors that in

50 s to produce interferon-gamma (IFNgamma) and granzyme B (GZB) in the absence of antigens, whereas con

51 a (IFNgamma), interleukin (IL)-6, IL-10, and granzyme B (GzB), with concurrent elevation of serum IFN

52 ls also acquire cytotoxic activity marked by granzyme B (GzmB) expression and the ability to promote

53 Granzyme B (GzmB) has previously been shown to be critic

54 Granzyme B (GzmB) is a serine protease involved in cell-

55 and the expression of CD107a(+) (LAMP1) and granzyme B (GZMB) on CD8(+) T cells.

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

57 th T-cell targets and was achieved through a granzyme B (GzmB)-dependent pathway.

58 okine induced by gamma interferon (MIG), and granzyme B (P <0.00001).

59 ll ratio was associated with higher baseline granzyme B (P = .0068; R(2) = 0.29) and degranulation po

60 ed cells is independent of caspases and that granzyme B activates the proapoptotic molecule Bid.

61 by infected CD4 T-cell elimination (ICE) and granzyme B activity did not significantly change over ti

62 ol that enables the in vivo visualization of granzyme B activity, a major effector of cytotoxic CD8+

63 by T cells are isolated using a reporter for granzyme B activity, and the antigens mediating recognit

64 Killer-cell granzyme B also activates caspase-independent pyroptosis

65 he most significantly upregulated gene, with granzyme B among the top five (log2 fold difference 3.58

66 Treatment with TLR8 agonists elicited granzyme B and also enhanced FcgammaR-mediated granzyme

67 uding CCR2 and CCR5), profound cytotoxicity (Granzyme B and CD107A), resistance to apoptosis (c-KIT a

68 th increased expression of IL-10, IL-17, and granzyme B and decreased expression of programmed death

69 antitumor capacity in vitro, with increased granzyme B and decreased PD-1 expression.

70 o define the functional activities of bovine granzyme B and determine its role in mediating the killi

71 tivation, but similar or decreased levels of granzyme B and effector cytokines.

72 al Ca(2+)-channel TRPML1, leads to increased granzyme B and enhanced functional potential, thereby mi

73 D1, CD30, ALK1, CD10, BCL6, perforin, TIA-1, Granzyme B and Epstein-Barr virus-encoded RNA.

74 erforin but require preactivation to express granzyme B and exert cytotoxicity.

75 D4 T cells had attenuated MVEC death through granzyme B and FasL.

76 earance and displayed enhanced expression of granzyme B and IFN-gamma by both virus-specific and tota

77 ceeded 1 x 107 HSV DNA copies, and surges in granzyme B and IFN-gamma occurred within the early hours

78 measured by proliferation and expression of granzyme B and IFN-gamma.

79 Helped T(EM) cells produce Granzyme B and IFNgamma upon antigen-independent, innate

80 ne activation could be detected by increased Granzyme B and Interferon gamma activity in the tumor as

81 CD8 + tumor-infiltrating T-cells expressing granzyme B and interferon gamma-1.

82 ry molecules CD23 and Bank1, and upregulated Granzyme B and Irf4, two molecules described as highly e

83 terminally differentiated profile, expressed granzyme B and maintained their ability to produce IFN-g

84 Ki-67+) CD8 T cells expressed high levels of granzyme B and PD-1, consistent with the profile of acut

85 NV-preexposed donors selectively upregulated granzyme B and PD1, unlike DENV-naive donors.

86 ry and activated maternal T cells expressing granzyme B and perforin are enriched at the maternal-fet

87 (+) T cells, with increased IFN-gamma, ICOS, granzyme B and perforin expression.

88 to calculate the spatiotemporal evolution of granzyme B and perforin from the time of their exocytosi

89 lpha production with IL-21 in CD4 or CD107a, granzyme B and perforin in CD8 T cells following stimula

90 The antibody-induced killer cells express, Granzyme B and Perforin that assault and kill other memb

91 pression of the cytotoxic effector molecules granzyme B and perforin; their degranulation upon exposu

92 dly undergo cytotoxic degranulation, release granzyme B and pro-inflammatory cytokines, leading to ta

93 dly undergo cytotoxic degranulation, release granzyme B and proinflammatory cytokines, leading to tar

94 Moreover, we found that IFNbeta induced granzyme B and promoted MRSA clearance in a granzyme B-d

95 nfection in vivo and increased expression of granzyme B and TNF upon stimulation with peptide Ag ex v

96 proteolytic cleavage, cleavages by casapses/granzyme B are considered as essential in the initiation

97 CGs are refilled with granzyme B at the late endosome stage and polarize to su

98 specifically activate their fluorescence by granzyme B but also passively target the tumor of living

99 activation of FcgammaR led to the release of granzyme B by AML cells.

100 d in upregulation of CD38, CD69, HLA-DR, and granzyme B by CD4(+) and CD8(+) T cells, and increased I

101 d that tofacitinib reduced the expression of granzyme B by CD8 T cells in vitro and in vivo systemic

102 a higher number of infiltrating IFNgamma and Granzyme B CD4 T cells and natural killer cells, and low

103 in using and/or developing tools for caspase/granzyme B cleavage prediction.

104 nformatics approaches and tools for caspases/granzyme B cleavage prediction.

105 Granzyme B cleaves a highly conserved set of proteins in

106 high) Jurkat cells released higher levels of Granzyme B compared with NKG2C(neg) NK cells and NKG2C(p

107 s using inhibitors specific for perforin and granzyme B confirmed that CD8(+) T cell killing of paras

108 Perforin/granzyme B content, degranulation (CD107a expression), a

109 cytokines; and NKT cell-derived perforin and granzyme B cytotoxins in promoting CD4(+) NKT cell ather

110 icle sensors of the activity of the protease granzyme B detect early T-cell-mediated rejection of tra

111 Extracellular granzyme B did not kill, but instead stimulated protease

112 ype in Foxp3(+) Treg cells and a decrease in granzyme B expression after Dll4 blockade.

113 mechanism implicated the down-regulation of Granzyme B expression and the essential involvement of L

114 These inhibitor effects resulted in reduced granzyme B expression by T cells, chemokine and intracel

115 human probe was able to specifically detect granzyme B expression in human samples, providing a clea

116 ures and location-specific features, such as granzyme B expression in the small intestine, revealing

117 ompared with blood CD8 T cells, with reduced granzyme B expression only in HIV(+) nonsmokers.

118 A marked differential in granzyme B expression was observed between treated respo

119 TGF-beta1 and granzyme B expression were also enriched within CD24(hi)

120 rly and Ag-independent IFN-gamma production, granzyme B expression, and degranulation.

121 ion (also a feature of lung TRM), maintained granzyme B expression, and did not equilibrate among imm

122 ion, but also gain IFN-gamma, TNF-alpha, and granzyme B expression.

123 sion of Kv1.3 correlated with high Ki-67 and granzyme B expression.

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

125 To assess the clinical value of a granzyme B imaging paradigm, biopsy specimens from melan

126 munoglobulin-like receptors (KIR) accumulate granzyme B in dense-core secretory lysosomes that conver

127 gulation of the cytotoxic markers CD107a and granzyme B in lung CD4(+), CD8(+), and MAIT cell populat

128 and cosecreted IL-13 and the killer protease granzyme B in response to allergen challenge.

129 well as the cytolytic proteins perforin and granzyme B in the infected mice.

130 further amplifies synthesis of IFN-gamma and granzyme B in the presence of otherwise weak innate stim

131 RM phenotype cells and reduced expression of granzyme B in the small intestine.

132 Such granzyme B induced in vivo signals of the reporters are

133 but not when neutrophils were depleted or a granzyme B inhibitor was added.

134 PET imaging probes for the murine and human granzyme B isoforms that specifically and quantitatively

135 CTL killing was also detected in FV-infected granzyme B knockout mice confirming that the exocytosis

136 Acquisition of KIR correlates with higher granzyme B levels and increased chemokine production in

137 om early viremic relapsers, correlating with granzyme B loading and effector multifunction.

138 HLA-G dimer targets Granzyme B pathway to prolong human renal allograft surv

139 Overall, our results suggest granzyme B PET imaging can serve as a quantitatively use

140 in decreased binding to Munc13-4 and delayed granzyme B polarization toward the immunologic synapse.

141 red by NK cells, and that the high levels of granzyme B produced in CL lesions was associated with la

142 terferon-gamma (21% [0.5%-28%]; P < .05) and granzyme B production (12.6% [7%-13.5%]; P < .05), and r

143 urvival while maintaining their cytokine and granzyme B production ability.

144 (+) T cells enhanced glycolytic capacity and granzyme B production as in CD8(+)CD28(-) T cells.

145 ation of macrophages and CD8+ T lymphocytes, granzyme B production by cytotoxic cells (cytotoxic T ce

146 anzyme B and also enhanced FcgammaR-mediated granzyme B production in an additive fashion.

147 , increased interferon-gamma (IFN-gamma) and granzyme B production in CD8(+) T cells and reduced TNFR

148 Cytotoxicity was demonstrated by granzyme B production in vitro and by in vivo killing of

149 activation (proliferation and IFN-gamma and granzyme B production) by beta-glucan-stimulated DCs in

150 FN-gamma production but not proliferation or granzyme B production).

151 d CD8(+) memory T-cell proliferation, higher granzyme B production, and expanded B-cell follicles cor

152 t enhances number, 41BB and GITR expression, granzyme B production, CTL/regulatory T cell ratio, and

153 an CD8 T cells resulted in higher number and granzyme B production, supporting the translational pote

154 CD69 expression and IFN-gamma, perforin, and granzyme B production, whereas NKT and mCD8(+) T cells s

155 ll effector functions, such as IFN-gamma and granzyme B production.

156 the HTLV-1 oncogene Tax, driven by the human granzyme B promoter (Tax(+)), develop osteolytic tumors.

157 of STAT4, resulting in direct binding at the granzyme B promoter within 2 h of exposure.

158 significantly correlated with the levels of granzyme B protein but not the levels of mRNA transcript

159 ct and quantify the expression of functional granzyme B protein.

160 of CD25 expression, as well as IFN-gamma and granzyme B secretion after allogeneic antigen stimulatio

161 Moreover, granzyme B secretion reduced in PBMC from TB-IRIS patien

162 IFN-gamma, cytotoxic activity, IFN-gamma and granzyme B secretion, and CD25 expression were measured

163 ched pathways included interferon signaling, granzyme B signaling and pathogen pattern recognition re

164 ites provide important insights into caspase/granzyme B substrate specificity, and facilitate the dis

165 independent data sets consisting of caspases/granzyme B substrates from different species and accordi

166 , we use differential proteomics to identify granzyme B substrates in three unrelated bacteria: Esche

167 ied, the complete repertoire of caspases and granzyme B substrates remains to be fully characterized.

168 y response and found that RTEs produced less granzyme B than their mature counterparts during infecti

169 which IL-12 and IL-7 synergistically control granzyme B through upregulation of the IL-12 receptor.

170 Polarization of granzyme B to the immunologic synapse and interaction of

171 This activation-driving cytokine release and Granzyme B upregulation-is TCR-independent but dependent

172 Furthermore, an in vitro blockade of granzyme B was observed to decrease TNF production.

173 , granular structures intensely positive for granzyme B were detected in association with T. gondii b

174 functional and nonfunctional forms of bovine granzyme B were produced, and the proteins expressed in

175 riments in pups, we showed that NK cells and granzyme B were required for IL-25 induction and activat

176 -box transcriptional factor Eomesodermin and granzyme B without loss of Foxp3 expression.

177 immune response, with decreased detection of granzyme B(+) and gamma interferon (IFN-gamma)(+) MAIT c

178 g-specific T cells with cytotoxic potential (granzyme B(+) CD107a(+)) targeting subdominant CE epitop

179 ward a CX3CR1(+) Eomesodermin(+) perforin(+) granzyme B(+) CD45RA(+) CD4 CTL phenotype.

180 Similarly, the number of granzyme B(+) cytotoxic CD8(+) alphabetaTCR(+) IELs incr

181 an increased frequency of tumor-infiltrating granzyme B(+) effector CD8 T cells and a reciprocal decr

182 our functions (IFN-gamma(+)IL-2(+)Perforin(+)Granzyme B(+)).

183 We observed granzyme B(+)/IFN-gamma(+), CD4(+), and CD8(+) prolifera

184 etect an immunoactivation-related biomarker (granzyme B) for real-time evaluation of cancer immunothe

185 of cytotoxic molecules (NKG2D, perforin, and granzyme B), and degranulation capacity of CD4(+)CD28(-)

186 te-macrophage colony-stimulating factor, and granzyme B), and they were able to kill autologous antig

187 Intracellular cytotoxic mediators (perforin/granzyme B), pro-inflammatory cytokines (IFNgamma/TNFalp

188 Intracellular cytotoxic mediators (perforin/granzyme B), proinflammatory cytokines (IFNgamma/TNFalph

189 As for CD8(+) T-cell activation (Perforin 1, Granzyme B).

190 r of the cytotoxic lymphocyte protease GzmB (granzyme B).

191 onuclear cells with IL-15 induced a cycling, granzyme B+ phenotype in CD8+ T cells.

192 ve an increased population of proliferating, granzyme B+, CD8+ T cells in circulation.

193 nvironment exhibited tumoral infiltration of granzyme B+CD8+ T cells (GzmB+CD8+ T cells), a type 1 IF

194 preclinical proof of concept for the use of granzyme B, a downstream effector of tumoral cytotoxic T

195 se line, which expresses a fusion protein of granzyme B, a key component of cytotoxic granules involv

196 in gB-elicited interferon-gamma (IFN-gamma), granzyme B, and CD107a and a reduction in lymphocyte act

197 nes and lytic factors, like soluble FasL and granzyme B, and eliminated the leukemic cells.

198 ater cytolytic activity, secreting perforin, granzyme B, and Fas ligand when activated.

199 , interferon (IFN)-gamma, CXCL9, Perforin 1, Granzyme B, and heat shock protein 60.

200 and CD25) and effector molecules (IFN-gamma, granzyme B, and IL-10) display organ-specific thresholds

201 cells while inducing the expression of CD39, granzyme B, and IL-10, resulting in the efficacious supp

202 terferon-gamma, tumor necrosis factor (TNF), granzyme B, and perforin than CD8+ T cells.

203 multaneously produced IFN-gamma, CD107(a/b), granzyme B, and perforin.

204 smaller amounts of cytotoxic molecules like granzyme B, and produced less interferon gamma than CD4

205 s containing proteins including perforin and granzyme B, are secreted into the synaptic cleft inducin

206 nel 2 included pancytokeratin, PD-1, CD45RO, granzyme B, CD57, FOXP3, and DAPI.

207 escent, and displayed high ex vivo levels of granzyme B, CX3CR1, CD38, or HLA-DR but less often coexp

208 ma, IL-10, IP-10, GM-CSF, sFasL, Granzyme A, Granzyme B, Granulysin, and Perforin following infection

209 tion of tetramer frequency and the levels of granzyme B, granzyme K, perforin, gamma interferon, tumo

210 An increase in perforin, granzyme b, IFNgamma, TNFalpha and a loss of GCR from th

211 An increase in perforin, granzyme B, IFNgamma, TNFalpha, and a loss of GCR from t

212 nscription factor T-BET to the gene encoding granzyme B, leading to increased transcription.

213 activation and senescence (e.g., IFN-gamma, Granzyme B, PD-1, KLRG1), and overproduce cytokines tied

214 olecules (TNFalpha, IFNgamma, interleukin 2, granzyme B, perforin, macrophage inflammatory protein 1b

215 increase expression of cytotoxic (IFNgamma, granzyme B, perforin-1, Fas ligand) and apoptotic (cleav

216 allograft tissue, where they are cleaved by granzyme B, releasing a fluorescent reporter that filter

217 ent up-regulation of FOXp3, CD39, IL-10, and granzyme B, resulting in enhanced suppressive activity o

218 along with upregulation of NKG2D, CD107, and granzyme B, suggesting cytotoxic function.

219 cognate receptor CXCR3, as well as CD8A and granzyme B, suggesting deficiencies in trafficking and/o

220 odial proteins were efficiently destroyed by granzyme B, suggesting proteolytic degradation of these

221 s were also more likely to express preformed granzyme B, suggesting that CD151+ T cells are pro-infla

222 tosis, involving the release of perforin and granzyme B, there is to date a lack of published informa

223 lar degradation of cytotoxic enzymes such as granzyme B, thus enhancing the cytotoxicity of T cells.

224 e substrate specific for the serine protease granzyme B, which is produced by recipient T cells durin

225 AIT cells, including increased production of granzyme B, which occurred before the onset of diabetes.

226 ytotoxic molecules perforin, granulysin, and granzyme B, which we termed polycytotoxic T cells.

227 cyte differentiation and function--including Granzyme B--are enriched among the genes that demonstrat

228 sulted in impaired accumulation of CTLA4 and granzyme B-containing intracellular vesicles at the IS,

229 ntly promote atherosclerosis by perforin and granzyme B-dependent apoptosis that increases postapopto

230 cutaneous leishmaniasis lesions and promotes granzyme B-dependent CD8 T-cell cytotoxicity.

231 granzyme B and promoted MRSA clearance in a granzyme B-dependent fashion.

232 Granzyme B-expressing B cells have been shown to be an i

233 Further studies showed that the granzyme B-mediated death of parasitized cells is indepe

234 (+) T cells led to enhanced infiltration and granzyme B-mediated destruction of developing tumors.

235 l of breast cancer, MLK3 inhibitor increases Granzyme B-positive CD8(+) T cells and decreases MLK3 an

236 e-producing MAIT cells were as frequent, but granzyme B-producing MAIT cells were more frequent upon

237 on with these peptides induced IFNgamma- and granzyme B-secreting CD4 T cells in response to autophag

238 ent on granule exocytosis and, specifically, granzyme B.

239 ptor CX3CR1, pro-inflammatory cytokines, and granzyme B.

240 ms that specifically and quantitatively bind granzyme B.

241 ath involves TNFalpha, Fas ligand (FasL) and granzyme B.

242 rofile producing high levels of IFNgamma and Granzyme B.

243 ed MVEC death involves in TNFalpha, FasL and granzyme B.

244 f genes encoding interferon-gamma, CD137 and granzyme B.

245 sion, and production of IFN-gamma, IL-2, and granzyme B.

246 necrosis factor alpha, gamma interferon, and granzyme B.

247 ction in the cytolytic granules perforin and granzyme B.

248 IFN-gamma production capacity and expressing granzyme B.

249 and associated negatively with expression of granzyme B.

250 tion gene 3, KLRG1, CD103, ICOS, CTLA-4, and granzyme B.

251 y B cells overexpressing the serine protease granzyme B.

252 ematic IFN-gamma, such as NKG2D, I-A(b), and granzyme B.

253 AIT cells also produced TNF-alpha, IL-2, and granzyme B.

254 lls and enhanced production of IFN-gamma and granzyme B.

255 ssion profiles, proliferation, and levels of granzyme B.

256 d SMAPs which contained TSP-1, perforin, and granzyme B.

257 ation on the biological activities of bovine granzyme B.

258 reased CTL effector function due to impaired granzyme B/perforin and Fas/Fas ligand pathways and a ph

259 ression was linked to CD4(+) T cells, whilst Granzyme B/TIA-1 to CD8(+) T cells.

260 hocytes expressing IFN-gamma, TNF-alpha, and granzyme B; these cells infiltrate tumors and induce reg

261 of CD69 and cytotoxic molecules perforin and granzyme B; we also observed a corresponding significant

262 , with an increase in CD8 T cells expressing granzyme-B and an increase in the CD8/Treg ratio compare

263 e to herpes simplex virus-1 (HSV-1), whereas granzyme-B induction upon IL-3/IL-10 stimulation was nor

264 ly to tumors, differentiate to IFN-gamma and granzyme-B secreting effector memory T cells but remain

265 ImmunoSpot assays yielded parallel results: granzyme-B with micro-cell-mediated lympholysis and inte

266 f cytotoxic effector molecules, perforin and granzyme beta, with reduced degranulation and CD57 expre

267 The strength of signaling for granzyme biosensors was dependent on perforin expression

268 Further development of caspase and granzyme biosensors will allow interrogation of addition

269 lls express gamma interferon (IFN-gamma) and granzymes but that granzymes are not required for sucras

270 s the cytolytic granule proteins perforin-A, granzyme C (GzmC), and GzmA and surface receptors IL-23R

271 Thus, inhibition of granzyme C effectively attenuated the killing.

272 Granule cytolytic perforin/granzyme C from this cell subsequently mediated cytotoxi

273 perforin, the mechanics of pore assembly and granzyme delivery remain unclear.

274 eath receptor-induced apoptosis and perforin/granzyme-dependent cytotoxicity.

275 not against peritoneal cells, in a perforin/granzyme-dependent manner.

276 lls by releasing cytolytic granule contents--granzyme (Gzm) proteases and the pore-forming perforin (

277 Granzymes have relatively broad and overlapping substrat

278 N-gammaR-deficient PLP-CD8 exhibited altered granzyme/IFN-gamma profiles, altered migration in recipi

279 Interestingly, Th22 cells also expressed granzymes, IL-13, and increased levels of Tbet.

280 erforin from the time of their exocytosis to granzyme internalization by the target cell.

281 nes to form pores that deliver pro-apoptotic granzymes into the target cell.

282 erforin) and pro-apoptotic serine proteases (granzymes) into the synaptic cleft.

283 ol gammaHV-associated lymphoma, but perforin/granzyme is a more potent effector mechanism for lymphom

284 identified a subpopulation of age-associated granzyme K (GZMK)-expressing CD8(+) T (Taa) cells that a

285 ors, we report development of granzyme A and granzyme K biosensors, for which no other functional rep

286 In the systemic compartment elevated Granzyme K expression was linked to CD4(+) T cells, whil

287 amer frequency and the levels of granzyme B, granzyme K, perforin, gamma interferon, tumor necrosis f

288 of interferon-gamma (IFN-gamma), but not by granzyme-mediated cytolytic activity.

289 rts their cytotoxic function through Fas and granzyme pathways.

290 pathologies from cancer to autoimmunity, the granzyme-perforin pathway has been the subject of extens

291 ulation and the inhibitory effect on Th1 and granzyme/perforin-related pathways.

292 ell effector functions, such as cytokine and granzyme production, depend on cytoplasmic Ca(2+), which

293 The cytotoxic granule granzyme proteases released by cytotoxic lymphocytes tri

294 on gamma (IFN-gamma) alone or dual IFN-gamma/granzyme rB producers is increased in breast milk compar

295 produce effector molecules such as IFNs and granzymes, their proliferation is inhibited during infec

296 pores facilitate the entry of pro-apoptotic granzymes, thereby rapidly killing the target cell.

297 fected mice use either IFN-gamma or perforin/granzyme to control gammaHV-associated lymphoma, but per

298 apse and thereby the release of perforin and granzymes toward the target cell.

299 produced IFN-gamma, TNF-alpha, perforin, and granzymes upon in vitro stimulation, demonstrating that

300 llular P. falciparum via the transfer of the granzymes, which was mediated by granulysin in a stage-s