ライフサイエンスコーパス: granzyme

1 s through the action of cytotoxic proteases (granzymes).

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

3 ntracellular Ca(2+) and to kill via perforin/granzyme.

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

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

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

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

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

9 Granzyme A deficiency resulted in an increased incidence

10 combinant protein Ag and GLA-SE also induces granzyme A expression in CD4 T cells and produces cytoly

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

12 Granzyme A is a protease implicated in the degradation o

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

14 ells, significantly diminished CD16, CD107a, granzyme A, and CD69 when in contact with GBM cells.

15 CD8(+) T cells expressing elevated levels of granzyme A, granzyme B, perforin, and IFN-gamma, we ther

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

17 d CD107a and secreted more soluble CD137 and granzyme A.

18 this cytolytic activity was not dependent on granzyme A/B or perforin.

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

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

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

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

23 Evidence is emerging that granzymes also play a role in controlling inflammation.

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

25 irement for spatiotemporal colocalization of granzyme and perforin acts as an effective bimolecular f

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

27 occurs in our model, a large amount of both granzyme and perforin still escape from the synapse.

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

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

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

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

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

33 Granzymes are serine proteases released by cytotoxic lym

34 se, and there was evidence for both perforin/granzyme as well as Fas/Fas ligand-dependent pathways of

35 n intersectin-1s (ITSN-1s) expression due to granzyme B (GrB) cleavage during inflammation associated

36 Human B cells express granzyme B (GrB) when cultured with IL-21, a cytokine ov

37 d that human pDC produce the serine protease granzyme B (GrB), thereby regulating T cell proliferatio

38 he accumulation of highly-differentiated and granzyme B (GrB)-expressing CD8(+)CD28(-) T cells has be

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

40 Importantly, we report that granzyme B (GzmB) contributes to this Treg resistance vi

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

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

43 The serine protease granzyme B (GzmB) is stored in the granules of cytotoxic

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

45 Granzyme B (GzmB) plays a major role in CTLs and NK cell

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

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

48 , 1.5-123; P = .011) and CD8 cells producing granzyme B (OR, 11; 95% CI, 1.9-212; P = .004) after P.

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

50 examethasone administration) in vivo reduced granzyme B activity (vehicle versus dexamethasone: 504+/

51 mor cell lysis associated with inhibition of granzyme B activity and Ca(2+) influx.

52 luorogenic substrate capable of reporting on granzyme B activity and examined its specificity ex vivo

53 Molecular imaging of granzyme B activity can visualize T cell-mediated myocar

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

55 In vivo experiments localized granzyme B activity in hearts with acute myocarditis mon

56 induced autophagy and subsequently increased granzyme B activity in target cells.

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

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

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

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

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

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

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

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

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

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

67 cific CD4 T cells can express high levels of granzyme B and kill target cells in an epitope- and orga

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

69 totoxic T cell (CTL) expressing perforin and granzyme B and of CTL producing IFN-gamma was augmented

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

71 The frequency of CD8(+) T cells producing granzyme B and perforin and those expressing inhibitory

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

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

74 of IFN-gamma in vivo and begin to accumulate granzyme B and perforin.

75 tibody also selectively enhancing release of granzyme B and perforin.

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

77 tease-cleavable luciferase biosensors detect granzyme B and pro-apoptotic caspase activation within m

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

79 Hence we have identified granzyme B as an important mediator of FcgammaR function

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

81 o) short-lived effector cells that expressed granzyme B at the tumor.

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

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

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

85 Granzyme B cleaves a highly conserved set of proteins in

86 nity, Prakash et al. (2014) demonstrate that granzyme B cleaves basement membrane proteins and promot

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

88 , IL-4, and IL-21 cytokines and perforin and granzyme B cytotoxins, CD4(+) NKT cells from mice defici

89 to prevent rejection injury from perforin or granzyme B effectors and enhanced PI-9 or SPI-6 expressi

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

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

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

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

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

95 ells localized to the lymph nodes, exhibited granzyme B expression, and conferred improved protection

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

97 l blocking of miR-23a in human CTLs enhanced granzyme B expression, and in mice with established tumo

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

99 ore cytotoxic phenotype, with high levels of granzyme B expression.

100 fficient to inhibit IFN-gamma production and granzyme B expression.

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

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

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

104 the NK cell expression of both IFN-gamma and granzyme B in response to flu infection.

105 blished a pivotal role for NK-cell NKG2D and granzyme B in the pathogenesis of HDM-induced allergic l

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

107 While the use of a granzyme B inhibitor decreased the number of apoptotic c

108 apoptosis and promotes the production of the granzyme B inhibitor protease inhibitor-9.

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

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

111 was the only population displaying elevated granzyme B levels and increased degranulation, although

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

113 c relapsers and reciprocally correlated with granzyme B loading, and CMV phosphoprotein 65 (pp65)-spe

114 T-cell receptor-expressing cells, diminished Granzyme B mRNA expression, and decreased caspase-3 acti

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

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

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

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

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

120 rotection from GVHD partly via inhibition of granzyme B production in CD8 T cells, whereas exposure o

121 Granzyme B production in CD8(+) T cells was higher in CL

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

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

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

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

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

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

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

129 ls to IL-2, IL-7, IL-15, and IL-21 increased granzyme B production.

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

131 ly correlated with IFN-gamma, TNF-alpha, and granzyme B production; T-bet and KLRG1 expression; proli

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

133 Granzyme B released by leukocytes cleaves multiple intra

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

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

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

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

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

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

140 the inability to deliver apoptosis-inducing granzyme B to target cells and to inhibition of NK-cell

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

142 ow that human monocytes produce the protease granzyme B upon both FcgammaR and TLR8 activation.

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

144 nct pattern of caspase activation induced by granzyme B versus Fas in human and murine CTLs.

145 toxicity markers, target cell apoptosis, and granzyme B were determined.

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

147 ls, the majority of which were CD27(+), were granzyme B(+) and made up about half of the dermal popul

148 meras had elevated Thy1, and there were less granzyme B(+) and Vgamma7(+) cells, indicating a greater

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

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

151 esence of higher frequencies of SIV-specific granzyme B(+) CD8 T cells within the lymphoid tissue, su

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

153 or (CCR)7(-) effector memory and perforin(+) granzyme B(+) cytotoxic cells, which express CD11a, CX3C

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

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

156 totoxic T cell-associated effector molecules granzyme B(+), IFN-gamma(+), TNF-alpha(+), and CCL3(+),

157 ation drove a >50-fold specific expansion of Granzyme B(high)/CD28(low)/CD57(high)/CD8(+) effector me

158 terleukin 2 [IL-2]) and cytolytic molecules (granzyme B) and reduced lung viral loads.

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

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

161 bodies against T cells (CD3, CD4, CD8, CD20, Granzyme B), CD68 (macrophages), and HLA-DR (human leuko

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

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

164 erleukin 2, tumor necrosis factor alpha, and granzyme B).

165 s encoding effector molecules (IFN-gamma and granzyme B).

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

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

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

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

170 icrobial and immunoregulatory functions, and granzyme B, a critical component of NK cell cytotoxic gr

171 racellular serpin that specifically inhibits granzyme B, a cytotoxic serine protease found in the cyt

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

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

174 lls secreted interferon gamma, perforin, and granzyme B, and expressed CD69, tumor necrosis factor-re

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

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

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

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

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

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

181 T cells expressing high levels of perforin, granzyme B, and T-bet.

182 results in elevated levels of IFN-gamma and granzyme B, as well as enhanced cytotoxicity.

183 lesions of NKG2D(+) CD8(+) T cells producing granzyme B, but surprisingly little IFN-gamma.

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

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

186 ssed by a combination of tetramer frequency, granzyme B, granzyme K, perforin, CD107(a/b) cytotoxic d

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

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

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

190 cription factor, Tbet, and the production of granzyme B, IL-22, and GM-CSF, with greater production o

191 t FHL1 is a target of the cytotoxic protease granzyme B, indicating that the generation of FHL1 fragm

192 es and can be cleaved by the serine protease granzyme B, one of the main components of cytotoxic gran

193 ls expressing elevated levels of granzyme A, granzyme B, perforin, and IFN-gamma, we therefore evalua

194 nd rapidly produce both interferon-gamma and granzyme B, providing significant pathogen protection in

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

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

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

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

199 optosis is reported to be a hallmark of both granzyme B- and Fas-mediated pathways of killing by CTLs

200 Recent evidence has identified the role of granzyme B- and perforin-expressing CD4(+) T cells with

201 activation was unexpectedly rapid following granzyme B- compared with Fas-mediated signal induction

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

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

204 adually after a 90-min delay in perforin- or granzyme B-deficient CTLs.

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

206 istic of their regulatory activity is direct granzyme B-dependent degradation of the TCR-zeta-chain,

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

208 Granzyme B-expressing regulatory B cells (GraB cells) ce

209 resistance of kidney TEC to cytotoxic T-cell granzyme B-induced death in vitro and in vivo is mediate

210 r epithelial cell expression of SPI-6 blocks granzyme B-mediated death because TEC from SPI-6 null ki

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

212 ied by an increased number of CD8(+)IFNgamma/granzyme B-producing effector T cells.

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

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

215 and associated negatively with expression of granzyme B.

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

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

218 y B cells overexpressing the serine protease granzyme B.

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

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

221 tment, and this enhancement of ADCC required granzyme B.

222 sed expression and secretion of perforin and granzyme B.

223 D and NK-cell effector functions mediated by granzyme B.

224 e expression of CD44, P-selectin ligand, and granzyme B.

225 cytokines as well as the cytolytic molecule granzyme B.

226 T cell-dependent intratumoral expression of granzyme B.

227 ic molecules, and efficiently delivers human granzyme B.

228 Clones secreted either FasL/IL-22 or granzyme B.

229 ory responses only if the NK cells expressed granzyme B.

230 or DNAM-1 and the lytic enzymes perforin and granzyme B.

231 rofile producing high levels of IFNgamma and Granzyme B.

232 sis factor-alpha, and the cytolitic protease granzyme B.

233 ry molecule-1 (DNAM-1; CD226), perforin, and granzyme B.

234 and produce significantly more IFN-gamma and granzyme B.

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

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

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

238 ms that specifically and quantitatively bind granzyme B.

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

240 ction in the cytolytic granules perforin and granzyme B.

241 IFN-gamma production capacity and expressing granzyme B.

242 , linked internally by either caspase 3/7 or granzyme B/caspase 8 cleavage sites, thus allowing activ

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

244 onger and differentiated into IFN-gamma- and granzyme-B (GrzB)-producing cytolytic Tc1-like effector

245 T cells from proliferating and upregulating Granzyme-B and interferon-gamma in response to tumor ant

246 hocytic infiltration and elevated IFN-gamma, granzyme-B and perforin intragraft.

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

248 ion of T-cell apoptosis by Fas-Fas ligand or granzyme-B pathways, and (iii) their capacity to produce

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

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

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

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

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

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

255 In Escherichia coli, granzymes cleave electron transport chain complex I and

256 C, accompanied by dynein-driven transport of granzyme-containing granules to and exocytosis at the co

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

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

259 attack by extravascular iNKT cells through a granzyme-dependent pathway, an observation also made in

260 s completed within 80 seconds, thus limiting granzyme diffusion.

261 still die, but more slowly, suggesting that granzymes disrupt multiple vital bacterial pathways.

262 The granzyme family serine proteases are key effector molecu

263 ve sufficient concentrations of perforin and granzyme for consistent pore formation and granzyme tran

264 Granzymes (Grs) are serine proteases mainly produced by

265 The physiological role of granzyme (Gzm) A is controversial, with significant deba

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

267 Killer lymphocyte granzyme (Gzm) serine proteases induce apoptosis of path

268 cells to kill target cells by perforin (Prf)/granzyme (Gzm)-induced apoptosis causes severe immune dy

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

270 However, the function of extracellular granzymes in inflammation largely remains unknown.

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

272 We used a metric of granzyme internalization to delineate which biological p

273 Here, we show that granulysin delivers granzymes into bacteria to kill diverse bacterial strain

274 rotein perforin is essential for delivery of granzymes into the cytoplasm of target cells; however th

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

276 icient for the delivery of lethal amounts of granzymes into the target cell.

277 ells, perforin delivers cytotoxic proteases (granzymes) into the target cell to trigger apoptosis.

278 Here, we show that granzyme K (GrK) binds to Gram-negative bacteria and the

279 Human granzyme K and the hepatitis C virus protease were also

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

281 mbination of tetramer frequency, granzyme B, granzyme K, perforin, CD107(a/b) cytotoxic degranulation

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

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

284 e for GzmA and/or the GzmB cluster, point to granzyme-mediated host defense regulation in the liver i

285 Conversely, the perforin/granzyme-mediated killing and IFN-gamma response of CD8-

286 over, a significant increase in perforin and granzyme mRNA expression was observed in PBMCs of infect

287 est (and best supported) model suggests that granzymes passively diffuse through the perforin pore in

288 recognition and killing through the perforin-granzyme pathway.

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

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

291 The cytotoxic granule granzyme proteases released by cytotoxic lymphocytes tri

292 Inhibitors of either granule function or granzyme proteolytic activity can arrest TCR-driven TEM,

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

294 Granzyme serum levels are elevated in patients with auto

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

298 d granzyme for consistent pore formation and granzyme transfer to target cells.

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

300 aining perforin, a pore-forming protein, and granzymes, which are proteases that induce apoptosis.