ライフサイエンスコーパス: FasL

1 FasL activity may play an active role in resolving eosin

2 FasL expression in the eye was increased with age, but d

3 FasL expression, BAL and tissue inflammatory cell and cy

4 FasL has been previously implicated in the pro-apoptotic

5 FasL interacted with Met through the FasL(105-130) extra

6 FasL is a transmembrane protein with a matrix metallopro

7 FasL may be a viable target for therapeutic intervention

8 FasL protein expression was examined in the eye and solu

9 FasL was recently shown be required for bacterial cleara

10 FasL-expressing human tumor cells express a significant

11 FasL-mediated cytotoxicity is one of the mechanisms that

12 may contribute to disease pathogenesis via a FasL-dependent mechanism that preferentially promotes le

13 ummary, SHED-mediated T-cell apoptosis via a FasL/Fas pathway results in immune tolerance and amelior

14 Thus, cDCs activate FasL-expressing T cells that regulate Fas-expressing ext

15 nse to Fas agonist in vitro and to activated FasL(+) T cells in vivo.

16 n mice 4 hours before or up to 2 hours after FasL injection resulted in a dramatic reduction of liver

17 ted the degree of calcium mobilization after FasL stimulation and found that LFG inhibits calcium rel

18 lling could be blocked by antibodies against FasL, which identified the Fas/FasL pathway as critical

19 ecessary for Tat-mediated protection against FasL apoptosis.

20 and Jurkat T-lymphocyte cells that although FasL activates both Akt and NF-kappaB, Akt inhibits FasL

21 sibility that heparin therapy may ameliorate FasL-mediated liver injury.

22 f B cells expressing IL-10 was present among FasL(+) B cells, but most FasL(+) B cells did not produc

23 greater p300-dependent H3K9 acetylation and FasL expression.

24 ng some cytotoxic activity as granzyme B and FasL are overexpressed and, while down-regulating T-bet,

25 attenuated MVEC death through granzyme B and FasL.

26 r (Th)2 cytokines, perforin, granzyme B, and FasL following drug stimulation.

27 tumor cells resistant to CD8(+) T cell- and FasL-mediated lysis, and tolerizes T cells by reverse si

28 and-death receptor pairs, i.e., TL1A-DR3 and FasL-Fas, were increased, as well as FADD and TRADD, and

29 d 9 ligands, increased expression of Fas and FasL in IECs in vitro.

30 with TLR ligands, and expression of Fas and FasL was investigated.

31 is finding, expression of intestinal Fas and FasL was reduced in vivo in the epithelium of TLR4 knock

32 ed the ratio of Bax/Bcl2 and induced Fas and FasL, initiated mitochondria- and death receptor-mediate

33 nd the expression levels of p75NTR, Fas, and FasL did not correlate with cell death.

34 mRNA expressions of TNF-alpha, IFN-gamma and FasL and increasing IL-10 mRNA expression.

35 ogs significantly increased CTL-mediated and FasL-induced apoptosis of colon carcinoma cells.

36 ll death of both lymphocytes and other APCs, FasL can also trigger the production of proinflammatory

37 SQ 22,536 restored BLT1(-/-) BMN apoptosis, FasL and CD36 expression, and clearance by macrophages.

38 ion of tumor-infiltrating CD8(+) T cells are FasL(+), and decitabine and vorinostat-mediated tumor-su

39 ays: by converting membrane-bound astrocytic FasL into a paracrine death signal for cancer cells, and

40 fusion and H(+)-ATPase apparently attenuated FasL-caused pH decrease.

41 l microvesicles carrying membranal bioactive FasL and TRAIL are formed and released in the extracellu

42 Our results suggest that bioactive FasL- and TRAIL-carrying exosomes, able to convey apopto

43 eas stimulation with CSup, derived from both FasL-overexpressing Jurkat cells and PBMC, could induce

44 Functional deficiency of Fas limits both FasL and ceramide analogs in the induction of apoptosis.

45 Evidence of both FasL and TRAIL-mediated signaling was seen after engagem

46 oteinase cleavage inactivates membrane-bound FasL and releases a soluble form reported to have both a

47 der light stress, soluble and membrane-bound FasL can bind to Fas, inducing apoptosis via a paracrine

48 mice express higher levels of membrane-bound FasL than do wild-type mice and fail to release soluble

49 triggered by cross-linked or membrane-bound FasL, CSup-derived stimuli-induced apoptosis exhibited u

50 Membrane-bound FasL, expressed by CD4(+) T cells, activated death recep

51 In this study, the role played by FasL expression in the cornea following acute infection

52 he immunosuppressive environment produced by FasL targeting correlated with reduced survival of tumor

53 tion of Fas prevents apoptosis stimulated by FasL as well as the Fas-activating antibody, CH11, as ev

54 dendritic cells (pDCs), IFN-I, and the CD95/FasL pathway, as targeted depletion or blockade of these

55 hanism that sensitizes ILC3s to undergo CD95/FasL-mediated apoptosis.

56 significant increase in Fas Ligand (CD95L) (FasL), CD69, and IL-R1 expression, and (2) skewed T-lymp

57 Fas allows osteosarcoma cells to circumvent FasL-mediated apoptosis upon entrance into the FasL(+) l

58 Constitutively FasL(+) B cells expressed higher levels of the IL-5 rece

59 ing Complex (DISC) components, and decreased FasL and CD36 expression.

60 n of ERp57 and GSTP1 substantially decreased FasL-induced oxidative processing and S-glutathionylatio

61 s, but not a Pla mutant (Deltapla), degrades FasL, which results in decreased downstream caspase-3/7

62 Thus, by degrading FasL, Y. pestis manipulates host cell death pathways to

63 V-1 could have developed strategies to delay FasL-mediated apoptosis in infected CD4(+) T lymphocytes

64 the intracellular expression of Tat delayed FasL-mediated apoptosis in both peripheral blood lymphoc

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

66 Ceramide enhances FasL-induced activation of the MAPK, NF-kappaB, and casp

67 prise a dual benefit: 1) storage of exosomal FasL and TRAIL in multivesicular bodies is protected fro

68 Wild-type bone marrow neutrophils expressed FasL and perforin, and when transferred to sensitized gl

69 lity, because it not only prevents extensive FasL-related liver injury but also limits the extent of

70 To determine to what extent FasL promotes inflammation in lupus mice, TMPD-injected

71 stern immunoblotting was used to detect Fas, FasL, sFasL, and caspase-3 expression in GCF.

72 osure did not elevate the expression of Fas, FasL, or the Fas-associated death domain adaptor protein

73 umor necrosis factor receptors (TNFRs): Fas, FasL, and TNFR superfamily member 1B.

74 Fas-FasL interactions primarily regulate T-cell homeostasis,

75 Fas-FasL-dependent activation-induced cell death (AICD) of T

76 influenza-specific CD8(+) T cells via a Fas-FasL-mediated pathway.

77 g that MDSC turnover may be regulated by Fas-FasL-mediated apoptosis.

78 We hypothesized that a cognate Fas-FasL interaction within the TME might limit both T cell

79 duced proliferation was not dependent on Fas-FasL- or tumor necrosis factor (TNF)-induced activation-

80 se to activated T cells, indicating that Fas-FasL regulation of myeloid cells was restricted to MDSCs

81 rease in MDSC survival is dependent upon Fas-FasL interactions, and this is consistent with gene expr

82 te potential cross-talk between TLRs and Fas/FasL system in intestinal epithelial cells (IECs).

83 is mediated by perforin/granzyme B- and Fas/FasL-mediated mechanisms.

84 lung epithelial apoptosis and decreased Fas/FasL expression compared to the control mice.

85 BTLA signaling limits Fas/FasL-mediated suppression of Listeria expansion within C

86 y blocking MPTP opening, DeltaPsim loss, Fas/FasL, and caspase activation.

87 sis, DeltaPsim loss, and upregulation of Fas/FasL/caspase.

88 This was accompanied by upregulation of Fas/FasL; Bax; and caspase-3, -8, and -9 activation.

89 ggests that it is linked to proapoptotic Fas/FasL signals.

90 tin attenuated apoptosis, down-regulated Fas/FasL signaling, suppressed intracellular reactive oxygen

91 Their strong Fas/FasL-mediated cytotoxicity and IFN-gamma response were s

92 odies against FasL, which identified the Fas/FasL pathway as critical cytotoxic mechanism during chro

93 Interestingly, the Fas/FasL pathway does play a role in regulatory T-cell deple

94 osis mediated by LPS and HIV through the Fas/FasL pathway, with key involvement of pDCs and type I IF

95 long with cell apoptosis and upregulated Fas/FasL/caspase expressions.

96 omoted T-cell apoptosis via upregulating Fas/FasL and caspase activities with a minimal effect on MPT

97 ead to skewed Treg composition in AA: first, FasL-mediated apoptosis on ligand interaction; and, seco

98 xpansion of a B cell population enriched for FasL(+) cells.

99 report here a novel signaling mechanism for FasL that hijacks the Met signal pathway to promote tumo

100 her, we uncovered that Fas, the receptor for FasL, is highly expressed on patient-derived T cells use

101 ld-type mice, suggesting a critical role for FasL in decitabine and vorinostat-mediated tumor suppres

102 These results disclose a new role for FasL in modulating immunosuppressive cells.

103 Consistent with a role for FasL in regulating immune responses, Deltapla infection

104 G protects only type II apoptotic cells from FasL-induced death in a Bcl-XL dependent manner.

105 following ovariectomy indistinguishably from FasL-intact controls, indicating that FasL is not a majo

106 Limiting the expression of functional FasL and TRAIL to exosomes comprise a dual benefit: 1) s

107 evels of the proapoptotic c-Jun target genes FasL and TNF-alpha.

108 Here, we studied the impact of host FasL on tumor development in mice.

109 Ectopic expression of human FasL in NIH3T3 cells significantly stimulated their migr

110 stablished tumors required neither IFNgamma, FasL, nor perforin by transferred CD8(+) T(E) cells targ

111 munoreactivity and proliferative activity in FasL-overexpressing animals compared with non-FasL-injur

112 ically, miR-mediated increased expression in FasL and Fas causing apoptosis and thymic atrophy.

113 - mice but was instead due to an increase in FasL+ DCs, resulting in IAV-specific CD4 T cell death.

114 In gld/gld mice with mutation in FasL, the beneficial effect of HDACIs on AICD of infiltr

115 as to whether LFG in the ER participates in FasL-induced death.

116 There was a sharp, near-simultaneous rise in FasL-induced intrahepatic apoptosis and coagulation, wit

117 tion of miR-18b and miR-23a led to increased FasL and Fas expression.

118 These results indicate FasL/perforin-independent functions of hapten-primed CD8

119 rostaglandin E2 (PGE2) cooperatively induced FasL expression in endothelial cells, which acquired the

120 Thus, alpha-GalCer-induced FasL/TRAIL and IL-33 provided a novel mechanism underlyi

121 rix metalloproteinase (MMP-7), which induced FasL expression in interstitial fibroblasts and potentia

122 tivates both Akt and NF-kappaB, Akt inhibits FasL-dependent NF-kappaB activity in a reactive oxygen s

123 es inflammation in lupus mice, TMPD-injected FasL-deficient and DeltaCS BALB/c mice were compared wit

124 the death ligand FasL, and capacity to kill FasL-sensitive tumors.

125 ells, surface expression of the death ligand FasL, and capacity to kill FasL-sensitive tumors.

126 gene encoding the apoptosis-inducing ligand FasL, is overexpressed within the majority of human tumo

127 dent expression of the death-receptor ligand FasL by iNKT cells was needed to restrict autoantibody p

128 The Fas receptor ligand FasL regulates immune cell levels by inducing apoptosis

129 Fas ligand (FasL) activity therefore should play a role in regulatin

130 r 3' untranslated regions of the Fas ligand (FasL) and Fas, respectively.

131 ed MVEC death involves TNFalpha, Fas ligand (FasL) and granzyme B.

132 lated their TRAIL in addition to Fas ligand (FasL) and induced alarm signaling molecule IL-33 in Kupf

133 -1-fluorobenzene (DNFB) required Fas ligand (FasL) and perforin expression.

134 late-stage cancer cells express Fas ligand (FasL) and show high malignancy with metastatic potential

135 ssengers, the TNF family members Fas ligand (FasL) and TRAIL in human early and term placentas.

136 Fas ligand (FasL) belongs to the TNF family of death ligands, and it

137 mma (IFNgamma), and particularly Fas ligand (FasL) by transferred CD8(+) effector T (T(E)) cells to r

138 in the genes that encode Fas or Fas ligand (FasL) can result in poor restraints on lymphocyte activa

139 dent regulation requires Fas and Fas ligand (FasL) expression by T cells, but not Fas expression by B

140 virus infection in mice enhances Fas ligand (FasL) expression on plasmacytoid dendritic cells (pDCs),

141 (Teffs), by up-regulating their Fas ligand (FasL) expression, which enabled them to kill Teffs throu

142 examined the effect of aging on Fas ligand (FasL) function in a mouse model of choroidal neovascular

143 Although Fas/Fas ligand (FasL) interactions have been strongly implicated in the

144 Fas ligand (FasL) is one potential target.

145 ased cell death surface receptor Fas ligand (FasL) level and caspase-8 activity in the cells; effects

146 Activation-induced Fas ligand (FasL) mRNA expression in CD4+ T cells is mainly controll

147 of the cornea is the presence of Fas ligand (FasL) on corneal epithelium and endothelium.

148 The Fas/Fas ligand (FasL) pathway modulates the balance of T cell subsets in

149 led to mB cell death via the Fas/Fas ligand (FasL) pathway.

150 the apoptotic signaling molecule Fas ligand (FasL) to prevent host cell apoptosis and inflammation.

151 y, educated NK cells upregulated Fas ligand (FasL) under these conditions.

152 ssociated with the expression of Fas ligand (FasL), a transmembrane protein that plays an important r

153 The role of Fas, and the Fas ligand (FasL), in the intestine is poorly understood.

154 Activated T cells secrete Fas ligand (FasL)-containing vesicles (secreted vesicles) that induc

155 ockdown sensitized BJAB cells to Fas ligand (FasL)-induced and Fas agonistic antibody-induced apoptos

156 Fas ligand (FasL)-induced apoptosis is augmented by S-glutathionylat

157 system that specifically blocks Fas ligand (FasL)-induced apoptosis.

158 nterferon-gamma (IFN-gamma)- and Fas ligand (FasL)-mediated apoptosis, resulting in hyporesponsivenes

159 T-cell apoptosis in OVX mice via Fas ligand (FasL)-mediated Fas pathway activation, leading to up-reg

160 Fas ligand (FasL)-mediated hepatocyte apoptosis occurs in the contex

161 egulate autoreactive B cells via Fas ligand (FasL).

162 decreased expression of Bax and Fas ligand (FasL).

163 r injury, but not by TNFalpha or Fas ligand (FasL).

164 -specific CD8+ T cells expressed Fas ligand (FasL).

165 expression of the death mediator Fas ligand (FasL, also called CD95L) in the vasculature of human and

166 the apoptosis-inducing molecule Fas ligand (FasL; CD178).

167 h receptor Fas and its physiological ligand (FasL) regulate apoptosis of cancerous cells, thereby fun

168 on of the death receptor Fas and its ligand, FasL.

169 nduced autoimmunity, and its cleavage limits FasL proinflammatory activity.

170 ced by Sorafenib with an increase of mouse(m)FasL and human(h)FasR expression.

171 However, in contrast to C57BL/6 mice, FasL is required for resolution of inflammation and prot

172 Age modulates FasL function where increased MMP cleavage leads to a lo

173 have elevated levels of cytotoxic molecules FasL, granzyme B, and perforin compared with their NKG2C

174 was present among FasL(+) B cells, but most FasL(+) B cells did not produce IL-10.

175 e ensuing induction of the calcineurin/NFAT, FasL/Fas, and caspase signaling cascades promote neonata

176 asL-overexpressing animals compared with non-FasL-injured littermates.

177 Notably, FasL variants activated the Met pathway, even though mos

178 t dictates the transcriptional activation of FasL under physiologic, as well as pathologic, condition

179 Blocking the activity of FasL or administration of caspase-8 inhibitor z-IETD inh

180 proapoptotic and proinflammatory activity of FasL, its cleavage site was deleted through targeted mut

181 T cells that was dependent on attenuation of FasL expression and led to CD8-dependent tumor growth su

182 Sevoflurane did not affect the binding of FasL to the extracellular domain of Fas receptor.

183 Furthermore, pharmacologic blockade of FasL protected the kidneys of wild-type mice from IRI.

184 een NF-kappaB and PI3K/Akt in the context of FasL signaling.

185 l effect was attributed to downregulation of FasL and to the induction of the antiapoptotic protein c

186 mice suggested that the pathogenic effect of FasL involves leukocytes; reconstitution of wild-type mi

187 The released form of FasL (sFasL) preferentially induces the migration of pro

188 Fas and a cleaved form of FasL were found on the cell surface of 661W cells.

189 To better understand the impact of FasL cleavage on both the proapoptotic and proinflammato

190 rus-infected mice, and that the induction of FasL expression on pDCs correlates with high levels of I

191 ion in MEF cells, resulting in inhibition of FasL-induced caspase 8 activation and apoptosis.

192 t and c-FLIP in the context of inhibition of FasL-induced NF-kappaB activity.

193 Knockdown of FasL expression by siRNA in DPSCs reduced their capacity

194 However, the expression level of FasL did not affect either DPSC proliferation rate or mu

195 h wild-type Y. pestis show reduced levels of FasL and activated caspase-3/7 compared to Deltapla infe

196 ith the pathologic increase in the levels of FasL mRNA.

197 The loss of FasL or inhibition of caspase activity alters host infla

198 n, Met phosphorylation, and cell motility of FasL(+) transfectants and tumor cells.

199 mice bearing a loss-of-function mutation of FasL (the gld mutation) and in wild-type mice.

200 ively characterized the surface phenotype of FasL(+) killer B cells, showing they are enriched in the

201 way and explains the metastatic phenotype of FasL-expressing tumors.

202 , the findings indicate that the presence of FasL on the cornea restricts the entry of Fas(+) bone ma

203 The down-regulation of FasL in these cells led to decreased Met activity and re

204 ablishes c-FLIP as an important regulator of FasL-mediated cell death.

205 these findings elucidate the relationship of FasL(+) B cells and IL-10-producing B cells and demonstr

206 We aimed to characterize the role of FasL expression in airway eosinophilia in Aspergillus fu

207 To study the role of FasL in induction of IL-2Ralpha(hi) NK cell death, a coc

208 is not seen, confirming the critical role of FasL regulation in the anti-tumor effect of HDACIs.

209 ice, genetic or pharmacologic suppression of FasL produced a substantial increase in the influx of tu

210 hepatitis is dependent on TRAIL, but not on FasL or TNFalpha.

211 ls, we examined the effect of sevoflurane on FasL-induced neutrophil apoptosis.

212 At the patient level, only FasL and disease status were significantly correlated (P

213 amma and lysis via cytotoxic granules and/or FasL.

214 we observed that deficiency of either Fas or FasL resulted in significantly increased incidence of 3-

215 Therefore, T(E) cells lacking IFNgamma or FasL cannot prevent progression of antigenic cancer beca

216 er, cytotoxic T(E) cells lacking IFNgamma or FasL could not prevent relapse despite retention of the

217 ene mutation of Fas (called lpr mutation) or FasL (called the gld mutation) prevents autoimmune diabe

218 ed after transfer of TNF-alpha, perforin, or FasL-deficient T cells.

219 anisms regulating physiologic and pathologic FasL transcription, TCR stimulation-responsive promoter

220 However, perforin/FasL double-knockout T cells failed to reject, arguing t

221 or GIMAP6, treatment with hydrogen peroxide, FasL, or okadaic acid significantly increased cell death

222 Consistently, placental FasL- and TRAIL-carrying exosomes triggered apoptosis in

223 ositive correlation was found between plasma FasL and HIV RNA levels and between Fas expression on mB

224 Postchallenge FasL gene expression in BAL cells and TUNEL positivity i

225 minant negative receptors (DNRs), preventing FasL-induced apoptosis in Fas-competent T cells.

226 In addition, proapoptotic (FasL, Bid, and activation of caspase-8 and caspase-3) an

227 Plasmacytoid dendritic cells (pDCs) produced FasL in response to HIV via binding to CD4 and chemokine

228 tosis-inducing human transmembrane proteins, FasL and TRAIL, synthesized and displayed on oil drops i

229 for AICD through suppressing NFAT1-regulated FasL expression on activated CD4(+) T cells.

230 lating OX-40 and Bcl-2 while down-regulating FasL and Bad expression, suggesting that similar to role

231 SA-FasL-engineered islet grafts established euglycemia in c

232 Most importantly, the transplantation of SA-FasL-engineered BALB/c islet grafts in conjunction with

233 igand protein chimeric with streptavidin (SA-FasL) and whether such engineered islets induce toleranc

234 otin following efficient engineering with SA-FasL protein that persisted on the surface of islets for

235 Active soluble FasL (sFasL) is detectable in the bronchoalveolar lavage

236 pression was examined in the eye and soluble FasL (sFasL) was measured in the blood.

237 ry cytokines and lytic factors, like soluble FasL and granzyme B, and eliminated the leukemic cells.

238 o wild-type mice and fail to release soluble FasL.

239 ammatory cell influx on day 1, while soluble FasL protein was released on day 7, preceding resolution

240 s showed a negative correlation with soluble FasL levels in the airways, MBP(+) eosinophils remained

241 ELISPOT analysis uncovered an Ag-specific FasL/IL-22-secreting T cell subset with skin-homing prop

242 ron receptor (IFNR) prevented HIV-stimulated FasL production in pDCs, HIV-plus-LPS-induced Fas expres

243 Strikingly, FasL but not perforin and granzymes were selectively act

244 In summary, FasL governs the immunoregulatory property of DPSCs in t

245 o diverse pancreatic and splenic suppressive FasL(high) B-cell subsets.

246 Systemic FasL neutralization significantly enhanced BAL and tissu

247 Genetically targeting FasL in naive mice increased myeloid cell populations, b

248 edge, LtxA is the first molecule, other than FasL, known to require the Fas death receptor to initiat

249 These results demonstrate that FasL promotes inflammation in TMPD-induced autoimmunity,

250 These data demonstrate that FasL, particularly on leukocytes, mediates ischemic AKI.

251 We found that FasL deficiency significantly reduced the early inflamma

252 However, we show herein that FasL-deficient mice lose bone mass following ovariectomy

253 y from FasL-intact controls, indicating that FasL is not a major contributor to the anti-osteoclastog

254 f the MDSC subset distribution revealed that FasL deficiency skewed cell populations toward the M-MDS

255 sing immunoelectron microscopy, we show that FasL and TRAIL are expressed on the limiting membrane of

256 iple inflammatory responses, suggesting that FasL may mediate ischemic AKI.

257 edge, we demonstrate for the first time that FasL and TRAIL are clustered on the exosomal membrane as

258 The FasL.2 allotype is expressed in BALB/c mice and exhibits

259 The FasL/IL-22-secreting clones expressed the skin-homing re

260 The FasL/perforin-mediated activity of wild-type neutrophils

261 inding, suggesting that nucleolin blocks the FasL-Fas interaction.

262 Collectively, our results establish the FasL-Met-Stat3 signaling pathway and explains the metast

263 l clearance in C57BL/6 mice that express the FasL.1 allotype.

264 g the phenotype and allowing survival in the FasL(+) lung microenvironment.

265 sL-mediated apoptosis upon entrance into the FasL(+) lung microenvironment.

266 g to FasL(117-126) significantly reduced the FasL/Met interaction, Met phosphorylation, and cell moti

267 e expression by RNAi technology reverted the FasL-associated motility to basal levels.

268 ion of Met and Stat3 activities reverted the FasL-associated phenotype.

269 cytes, and heparin-treated mice survived the FasL-induced liver injury longer compared with heparin-u

270 FasL interacted with Met through the FasL(105-130) extracellular region in lipid rafts, which

271 tis in BALB/c mice is not dependent upon the FasL.

272 splayed the most severe disease, whereas the FasL-defective gld mouse displayed an intermediate pheno

273 the Fas and TLR signaling pathways, with the FasL/Fas system playing a role in TLR-mediated inflammat

274 ll-mediated MVEC death involves in TNFalpha, FasL and granzyme B.

275 als received either neutralizing antibody to FasL (clone MFL4) or irrelevant hamster IgG via intraper

276 ogenous C16 ceramide sensitized CML cells to FasL-induced apoptosis, whereas overexpression of A-CDas

277 he metastatic human colon carcinoma cells to FasL-induced apoptosis.

278 on and increased sensitivity of CML cells to FasL-induced apoptosis.

279 sitization of human colon carcinoma cells to FasL-induced apoptosis.

280 nction to sensitize colon carcinoma cells to FasL-induced apoptosis.

281 ent with synthetic peptides corresponding to FasL(117-126) significantly reduced the FasL/Met interac

282 IL-15 withdrawal led to FasL-dependent killing of IL-2Ralpha(hi) NK cells by mor

283 A-CDase decreased CML cells' sensitivity to FasL-induced apoptosis.

284 ased Fas expression and their sensitivity to FasL.

285 2 cells and thus in decreased sensitivity to FasL.

286 n proteins in which a soluble form of TRAIL, FasL or CD40L is genetically fused to a high-affinity an

287 y because of liver damage triggered by TRAIL/FasL.

288 Finally, the transfectants of truncated FasL showed strong anchorage-independent growth and lung

289 In these tumors, FasL expression was associated with scarce CD8(+) infilt

290 tion was antigen-specific and dependent upon FasL.

291 that LAT-deficient CTLs failed to upregulate FasL and produce gamma interferon after engagement with

292 Furthermore, tumor-bearing mice that were FasL-deficient displayed an enhanced proportion of tumor

293 duced sensitization and to determine whether FasL neutralization alters the inflammatory response.

294 ha(hi) NK cell death, a coculture assay with FasL-blocking Abs was used.

295 Engagement of Fas with FasL triggered NF-kappaB activation.

296 Heparin did not directly interfere with FasL-induced apoptosis in isolated hepatocytes, and hepa

297 D-gld/+) or treating NOD-wild-type mice with FasL-neutralizing monoclonal antibody completely prevent

298 Stimulation with FasL rapidly induced associations of Fas with ERp57 and

299 661W cells were treated with FasL or Fas agonistic antibody, or exposed to light with

300 Treatment with FasL or Fas agonistic antibody induced apoptosis in 661W