ライフサイエンスコーパス: Fas ligand

1 scripts for perforin and granzyme B, but not Fas ligand.

2 d apoptosis in response to TNF-alpha but not Fas ligand.

3 . murina led to increased lung expression of Fas ligand.

4 t with agonistic Abs or cross-linked soluble Fas ligand.

5 interleukin 8, tumor growth factor beta, and Fas ligand.

6 actor-related apoptosis-inducing ligand, and Fas ligand.

7 T cells by down-regulating the expression of Fas ligand.

8 tion transduced by reverse signaling through Fas ligand.

9 turn requires MEK2 activity and secretion of FAS ligand.

10 the immediate expression of the proapoptotic Fas ligand.

11 as, the receptor that mediates the action of Fas ligand.

12 D3 decreased apoptosis induced by TRAIL and Fas ligand.

13 rs them responsive to receptor engagement by Fas ligand.

14 "FAS-re-expression" and are augmented by the FAS-ligand.

15 cell expression of IL-4, IL-10, perforin, or Fas ligand; 2) could not be reversed by IL-2, IL-7, or I

16 Cholesterol depletion, after Fas ligand activation of apoptosis, reduced raft formati

17 the usual markers, including plasma soluble FAS ligand and an in vitro apoptotic defect.

18 ut the susceptibility of cells to killing by Fas ligand and anti-Fas antibodies is highly variable.

19 ons in gld.apoE-/- mice that lack functional Fas ligand and apolipoprotein E and exhibit accelerated

20 cells with other stress inducers, including Fas ligand and buthionine sulfoxide, also induced Bcl-2

21 In rat islets, constitutive expression of Fas ligand and glucose-induced Fas receptor expression w

22 1.1+ cells and is dependent on IFN-gamma and Fas ligand and independent of perforin.

23 n significant elevation in the expression of Fas ligand and intracellular p21 levels, expression of S

24 3/6(+) and were variably enriched in 42-kDa Fas ligand and MHC class I but not class II molecules.

25 cells and containing killer proteins (i.e., Fas ligand and perforin molecules).

26 expansion, but expressed significantly less Fas ligand and produced significantly lower levels of IF

27 ules secondary lymphoid tissue chemokine and Fas ligand and the costimulatory molecules 4-1BBL and TN

28 This subset, which also includes Fas ligand and TNF-alpha, can activate the extrinsic apo

29 The FOXO3a target genes Fas ligand and TRAIL, involved in the extrinsic apoptoti

30 vity and enhancing the apoptotic activity of Fas ligand and TRAIL.

31 l human astrocytes from apoptosis induced by Fas ligand and TRAIL.

32 uction of apoptosis by death ligands such as Fas ligand and tumor necrosis factor-alpha-related apopt

33 ression of death receptor ligands, including Fas ligand and tumor necrosis factor-related apoptosis-i

34 and its inhibition leads to sensitization to Fas ligand and tumor necrosis factor-related apoptosis-i

35 ter, Foxo3a-deficient neutrophils upregulate Fas ligand and undergo apoptosis in response to TNF-alph

36 Autocrine secretion of FAS ligand and upregulated FAS expression induced by UVB

37 eak of plasma viral load (VL), while TNFR-2, Fas ligand, and microparticle level elevations occurred

38 associated with marked upregulation of FAS, FAS ligand, and the adaptor molecules RIPK1 and CFLAR.

39 of the inhibition of the expression of Fas, Fas ligand, and the mammalian death adaptor protein term

40 ia binding of its Fas moiety to cell surface Fas ligand, and then to allow the Fc moiety to invoke it

41 cells, including IFN-gamma, perforin, TRAIL, Fas ligand, and TNF-alpha.

42 ted by the absence of caspase-1, caspase-11, Fas ligand, and TNF.

43 AMCase protects airway epithelial cells from Fas ligand- and growth factor withdrawal-induced apoptos

44 bit multiple effector activities, perforin-, Fas ligand-, and TRAIL-mediated cytotoxicity, and secret

45 ls were all mitigated in septic Fas(-/-) and Fas ligand(-/-) animals.

46 Transcripts of Fas ligand are abnormally increased in autoimmune hepati

47 Death induction and costimulation by Fas ligand are therefore clearly separable functions.

48 ying beta-cells were limited to perforin and Fas ligand, as double knockouts of these molecules abrog

49 6) or mice with a functional mutation in the Fas ligand (B6.gld) were given either high-fat control d

50 To our surprise, in the absence of Fas ligand, BALB(gld) mice showed no difference in bacte

51 rotein also suppresses apoptosis mediated by Fas ligand because of c-Jun-dependent Fas down-regulatio

52 vitality during inflammation by suppressing Fas ligand; because Foxo3a can bind and suppress the Fas

53 tosis in response to TNF-alpha and IL-1, and Fas ligand blockade renders Foxo3a-deficient mice suscep

54 ases by Fas when treated with membrane-bound Fas ligand, but not with agonistic Abs or cross-linked s

55 CD40 activation of DC via high expression of Fas ligand by the Vdelta1 T cells.

56 ell-cell contact-dependent manner, involving Fas-ligand (CD95L).

57 forin but expressed higher levels of Fas and Fas ligand, compared with their counterparts in peripher

58 -negative T-cell counts and plasma IL-10 and FAS ligand concentrations were determined as ALPS marker

59 A modest role for perforin but not for Fas/Fas ligand could be demonstrated.

60 Here we report on the first case of complete FAS ligand deficiency caused by a homozygous null mutant

61 FAS ligand deficiency should be screened in patients pre

62 of T1 black hole volume (P = .002), whereas Fas ligand-deficient mice did not (P = .77).

63 However, in IFN-gamma- or Fas ligand-deficient mice, but not T cell-deficient mice

64 Using Fas ligand-deficient or TRAIL-deficient DLI had no impac

65 tuted with wild-type, perforin-deficient, or Fas ligand-deficient T(reg).

66 ells were more sensitive to Ca-dependent and Fas ligand-dependent killing by cytotoxic T lymphocytes.

67 T cells and induced their apoptosis in a Fas/Fas ligand-dependent manner.

68 death via activation of Caspase-8 through a Fas ligand-dependent mechanism.

69 ce for both perforin/granzyme as well as Fas/Fas ligand-dependent pathways of killing by NK cells.

70 death of infected cells through perforin- or Fas ligand-dependent pathways.

71 ceptor, is activated by the membrane protein Fas ligand expressed on various immune cells.

72 we previously reported increased numbers of Fas ligand expressing CD8(+) T lymphocytes in the septic

73 pithelial cells against apoptosis, decreased Fas ligand expression and also improved survival.

74 caIKKbeta T cells showed increased Fas ligand expression and caspase-8 activation, and bloc

75 an nuclear receptor ROR-gammat but increased Fas ligand expression and died by apoptosis.

76 group, treatment with dexamethasone reduced Fas ligand expression and significantly improved surviva

77 evidence for transcriptional control of the Fas ligand expression by NF-kappaB was sought.

78 apoptosis and attenuated CLP-induced Fas and Fas ligand expression in the myocardium.

79 in HIVAN is mediated by NF-kappaB-activated Fas ligand expression was investigated here.

80 overexpression increased cell apoptosis and Fas ligand expression, compared with STAT1 beta overexpr

81 ators of death receptor-dependent apoptosis (Fas ligand, Fas, and caspase 4), p53-like proteins (p73,

82 MX3350-1 increased the levels of Fas-ligand, Fas, and Fas-associated death domain, and en

83 CTL activity was also independent of the Fas ligand-Fas, TRAIL-DR5, and canonical death pathways,

84 s independent of both CD8(+) T cells and the Fas ligand/Fas pathway, and is not explained by a lack o

85 signaling in human T and NK cells initiates Fas ligand/Fas-mediated caspase-3/-7 activation and resu

86 Fas ligand (FasL) activity therefore should play a role

87 factor-related apoptosis-inducing ligand, or Fas ligand (FasL) alone were critical for in vivo effica

88 node (LN) dendritic cells (DCs) that express Fas ligand (FasL) and drive FasL-Fas (DC-T)-induced apop

89 affinity for 3' untranslated regions of the Fas ligand (FasL) and Fas, respectively.

90 cell-mediated MVEC death involves TNFalpha, Fas ligand (FasL) and granzyme B.

91 of biologically active components, including Fas ligand (FasL) and HLA-DR, than those from pregnancie

92 cells upregulated their TRAIL in addition to Fas ligand (FasL) and induced alarm signaling molecule I

93 n to effects on GrB, VIP also down-regulates Fas ligand (FasL) and perforin (Pfr) expression.

94 2,4-dinitro-1-fluorobenzene (DNFB) required Fas ligand (FasL) and perforin expression.

95 Many late-stage cancer cells express Fas ligand (FasL) and show high malignancy with metastat

96 This results in upregulation of FAS ligand (FASL) and subsequent apoptosis through the F

97 ear factor kappaB ligand (RANKL), TNF-alpha, Fas ligand (FasL) and TNF-related apoptosis-inducing lig

98 ant death messengers, the TNF family members Fas ligand (FasL) and TRAIL in human early and term plac

99 (+)CD4(+) T cells that produced the cytokine Fas ligand (FasL) as a result of NKG2D costimulation but

100 vitro expression studies identified FAS and FAS ligand (FASL) as potential mediators of this phenome

101 Fas ligand (FasL) belongs to the TNF family of death lig

102 through up-regulation of the death receptor Fas ligand (FasL) by HIV-1 negative factor (Nef), leadin

103 orin, IFN-gamma (IFNgamma), and particularly Fas ligand (FasL) by transferred CD8(+) effector T (T(E)

104 Fas ligand (FasL) can be either membrane bound, or cleav

105 Mutations in the genes that encode Fas or Fas ligand (FasL) can result in poor restraints on lymph

106 Fas ligand (FasL) causes apoptosis of epidermal keratino

107 The biological relevance of the perforin and Fas ligand (FasL) cytolytic pathways of CD8(+) T lymphoc

108 Fas ligand (FasL) exerts potent proapoptotic and proinfl

109 at cDC-dependent regulation requires Fas and Fas ligand (FasL) expression by T cells, but not Fas exp

110 ption factor that has been found to regulate Fas ligand (FasL) expression during activation-induced T

111 ethal H5N1, virus infection in mice enhances Fas ligand (FasL) expression on plasmacytoid dendritic c

112 ctor T cells (Teffs), by up-regulating their Fas ligand (FasL) expression, which enabled them to kill

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

114 Recent studies have suggested a role for Fas ligand (FasL) in estrogen-induced osteoclast apoptos

115 The critical role played by Fas ligand (FasL) in immune homeostasis renders this mol

116 Recent findings have implicated Fas/Fas ligand (FasL) in mediating the death of keratinocyte

117 P down-regulation and apoptosis induction by Fas ligand (FasL) in primary lung epithelial cells.

118 tolerogenic, initially suggesting a role for Fas ligand (FasL) in tolerance.

119 study, we demonstrate that stimulation with Fas ligand (FasL) induces S-glutathionylation of Fas at

120 tes (NCM460) and of PGE(2) or toxin A on the Fas ligand (FasL) induction were analyzed by flow cytome

121 Fas/Fas ligand (FasL) interaction plays a critical role in i

122 Although Fas/Fas ligand (FasL) interactions have been strongly implic

123 ouse survival, little is known about how Fas-Fas ligand (FasL) interactions mediate this protection a

124 study, we evaluated the contribution of Fas-Fas ligand (FasL) interactions to CD8+ T-cell-mediated c

125 Fas ligand (FasL) is a 40-kDa type II transmembrane prot

126 Fas ligand (FasL) is a major immune effector molecule th

127 Interaction of Fas with Fas ligand (FasL) is known to play a role in peripheral

128 Fas ligand (FasL) is one potential target.

129 Although Fas ligand (FasL) is primarily expressed by lymphoid cel

130 F also increased cell death surface receptor Fas ligand (FasL) level and caspase-8 activity in the ce

131 Activation-induced Fas ligand (FasL) mRNA expression in CD4+ T cells is mai

132 By engaging Fas, Fas ligand (FasL) on activated T lymphocytes induces act

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

134 ate that IAP antagonists in combination with Fas ligand (FasL) or the death receptor 5 (DR5) agonist

135 th doxycycline (Dox)-dependent lung-specific Fas ligand (FasL) overexpression, treated with Dox betwe

136 The Fas/Fas ligand (FasL) pathway modulates the balance of T cel

137 Apoptosis via the Fas/Fas ligand (FasL) pathway plays an important role in the

138 is of cardiac allograft myocytes through Fas/Fas ligand (FasL) pathway.

139 LPS and HIV led to mB cell death via the Fas/Fas ligand (FasL) pathway.

140 denoviral vectors expressing IL-10, IL-4, or Fas ligand (FasL) produce anti-inflammatory exosomes abl

141 ince we previously demonstrated that the Fas/Fas ligand (FasL) system is involved in paracrine-mediat

142 tumors expressing the membrane-only form of Fas ligand (FasL) terminate immune privilege, induce vig

143 la degrades the apoptotic signaling molecule Fas ligand (FasL) to prevent host cell apoptosis and inf

144 Conversely, educated NK cells upregulated Fas ligand (FasL) under these conditions.

145 ed TRAIL, which in concert with perforin and Fas ligand (FasL) was involved in the tumor-specific CTL

146 lation was associated with the expression of Fas ligand (FasL), a transmembrane protein that plays an

147 mediate downstream target, the death-inducer Fas ligand (FasL), and its cognate receptor Fas.

148 myeloma cells via MHC class I, perforin, and Fas ligand (FasL), and Th1, but not Th2, cells lysed the

149 dition, we have demonstrated a role for Fas, Fas ligand (FasL), and TRAIL in promoting Th2 developmen

150 characterized for their expression of CD70, Fas ligand (FasL), and tumor necrosis factor-alpha (TNF-

151 RENCA activity is dependent on IFN-gamma and Fas ligand (FasL), but does not require soluble or membr

152 factors are involved in the up-regulation of Fas ligand (FasL), FasL mRNA was quantified and found to

153 ury to the retina, IL-10 was upregulated and Fas ligand (FasL), IL-12, and TNF-alpha were downregulat

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

155 s has recently been shown to be regulated by Fas ligand (FasL), its role in beta-glucan activation of

156 The AECs expressed message for TNFalpha, Fas ligand (FasL), TRAIL (tumor necrosis factor-related

157 Furthermore, a Fas ligand (FasL)-blocking antibody significantly inhibi

158 Activated T cells secrete Fas ligand (FasL)-containing vesicles (secreted vesicles

159 tibody production is T cell-dependent in Fas/Fas ligand (FasL)-deficient (lpr/lpr or gld/gld) mice.

160 s induced transient T cell apoptosis via the FAS ligand (FASL)-dependent FAS pathway and could amelio

161 Fas ligand (FasL)-Fas engagement proved important in thi

162 Nucleolin knockdown sensitized BJAB cells to Fas ligand (FasL)-induced and Fas agonistic antibody-ind

163 We have studied this issue using Fas ligand (FasL)-induced apoptosis in Jurkat cells wher

164 n GSH transport and ionic homeostasis during Fas ligand (FasL)-induced apoptosis in Jurkat cells.

165 Fas ligand (FasL)-induced apoptosis is augmented by S-gl

166 the nervous system that specifically blocks Fas ligand (FasL)-induced apoptosis.

167 Fas/Fas ligand (FasL)-mediated apoptosis plays a critical ro

168 en-driven, interferon-gamma (IFN-gamma)- and Fas ligand (FasL)-mediated apoptosis, resulting in hypor

169 s activated T-cell apoptosis in OVX mice via Fas ligand (FasL)-mediated Fas pathway activation, leadi

170 Fas ligand (FasL)-mediated hepatocyte apoptosis occurs i

171 In vivo, we observed perforin- and Fas ligand (FasL)-mediated reduction of donor T cell pro

172 ed on chromosome 10 (PTEN), but also targets Fas ligand (FasL).

173 , NK receptor group 2, member D (NKG2D), and Fas ligand (FasL).

174 tain cells expressing high levels of Fas and Fas ligand (FasL).

175 s (LPL), and these activated cells expressed Fas ligand (FasL).

176 mpanied by a decreased expression of Bax and Fas ligand (FasL).

177 g acute liver injury, but not by TNFalpha or Fas ligand (FasL).

178 ucing activated T-cell apoptosis through the FAS ligand (FASL)/FAS-mediated death pathway via cell-ce

179 mining the effects of 2-methoxyestradiol and Fas ligand (FasL)/tumor necrosis factor-related apoptosi

180 ular adhesion molecule-1 (ICAM-1, 1548 A>G), Fas ligand (fasL, -844 C>T), inducible costimulator (ICO

181 d selective expression of the death mediator Fas ligand (FasL, also called CD95L) in the vasculature

182 Fas ligand (FasL/CD95L), a member of the tumor necrosis

183 xpression of the apoptosis-inducing molecule Fas ligand (FasL; CD178).

184 ic anemia patients show up-regulated Fas and Fas-ligand (FasL) expression, respectively, supporting a

185 of aryl hydrocarbon receptor (AhR), Fas, and Fas-ligand (FasL) expression.

186 y were to generate conditional lung-specific Fas-ligand (FasL) transgenic mice and to determine the e

187 o an apoptotic program by cross-linking with Fas-ligand (FasL).

188 FAS ligand function was assessed based on reactivation-i

189 scribed in patients with ALPS, including the FAS ligand gene (FASLG) in rare cases.

190 ralization of tumor necrosis factor alpha or Fas ligand had no effect on apoptosis.

191 ntial role of cell cycle regulators, such as Fas ligand, has been examined in the etiology of bile du

192 reas Tgfb1(-/-) CD4(+) T cells overexpressed Fas ligand, hepatocellular damage was observed in Fas(lp

193 Its known ligands include Fas ligand, homologous to lymphotoxin, showing inducible

194 pression of the apoptosis-triggering protein Fas ligand in pro-B cells.

195 is in HIVAN by controlling the expression of Fas ligand in renal epithelium.

196 ting agents were found to synergize with the FAS-ligand in inducing apoptosis in neoplastic MCs.

197 ostimulation, casein kinase I phosphorylates Fas ligand, in which two conserved casein kinase I bindi

198 The fatal responses were perforin- and Fas ligand-independent, and were associated with high se

199 Tumor necrosis factor-alpha (TNF-alpha) and Fas ligand induce apoptosis by interacting with their co

200 spliced LR transcripts inhibit cold shock or Fas ligand-induced apoptosis in mouse neuroblastoma (neu

201 tion in the CNS and disease recovery via Fas/Fas ligand-induced apoptosis of encephalitogenic T cells

202 by our demonstration of cadmium chloride- or Fas ligand-induced apoptosis resistance in circulating m

203 ial cells from growth factor withdrawal- and Fas ligand-induced apoptosis.

204 g primary T lymphocytes are resistant to Fas/Fas ligand-induced apoptosis.

205 t syndecan member also led to an increase in Fas ligand-induced apoptosis.

206 following chloride flux modulation, whereas Fas ligand-induced apoptotic characteristics are not aff

207 Type I signaling involves Fas ligand-induced recruitment of large amounts of FADD

208 HIV-1 gp120-induced apoptosis by regulating Fas ligand induction and activation of the phosphoinosit

209 icient, DISC complexes, while membrane-bound Fas ligand initiates a smaller but more efficient DISC t

210 gnaling complex formation in response to Fas/Fas ligand interaction.

211 ically kill activated OT-I cells through Fas/Fas ligand interaction.

212 n of apoptosis of GC-B cells through the FAS/FAS-ligand interaction.

213 n and caspase-8 activation, and blocking Fas/Fas ligand interactions enhanced cell survival.

214 d synthesis in scar tissue and mediating Fas-Fas ligand interactions.

215 induce neutrophil apoptosis through Fas and Fas-ligand interactions, and aberrant B-cell reconstitut

216 f cholangiocarcinoma cells recruited Fas and Fas ligand into the lipid rafts, subsequently activating

217 d cells with an agonistic anti-Fas antibody, Fas ligand, irradiation, and tumor necrosis factor-relat

218 Fas ligand is one such molecule whose cell surface expre

219 cells using transgenic Mafia mice, in which Fas ligand is selectively activated in these cells, resu

220 The cytoplasmic domain of Fas ligand is sufficient to costimulate CD8(+) T cells b

221 of IRF-1 and proapoptotic molecules such as Fas ligand, its receptor (Fas) and death receptor 5, whi

222 FAS-induced apoptosis was normal, and plasma FAS ligand levels were not detectable.

223 , malondialdehyde, protein carbonyl, and Fas/Fas ligand levels.

224 rthologs of BAFF, APRIL, EDA, TWEAK, 4-1BBL, Fas ligand, LIGHT, CD40L, RANKL, and possibly TL1A; 2) t

225 opment, both SMA lines showed an increase in Fas ligand-mediated apoptosis and increased caspase-8 an

226 eceptor 1/receptor 2 (DR4/DR5) levels and to Fas ligand-mediated apoptosis via up-regulation of surfa

227 All the proteins reduced levels of Fas ligand-mediated apoptosis, reducing the activity of

228 he anterior chamber (AC) of the eye required Fas ligand-mediated apoptotic death of inflammatory cell

229 scein-conjugated anti-Fas antibody abrogated Fas ligand-mediated caspase activation.

230 T cells by decreasing susceptibility to Fas/Fas ligand-mediated cell death.

231 Further, upon Fas ligand-mediated costimulation, casein kinase I phosp

232 ymphocytes express perforin-mediated and Fas/Fas ligand-mediated cytotoxicity.

233 e apoptotic due to the activation of the Fas-Fas ligand-mediated extrinsic pathway.

234 iggered an immunopathologically limiting Fas-Fas-ligand-mediated apoptotic pathway in lamina propria

235 We now show that Fas ligand molecules lacking amino acids 45-54 in the pr

236 ide inhibitor could reduce the expression of Fas ligand mRNA in HIVAN podocytes.

237 ion of caspases 8 and 3 and up-regulation of Fas ligand mRNA, whereas calpain-mediated cell death dep

238 ucing ligand (TRAIL), TRAIL-R(DR5), Fas, and Fas ligand mRNAs and/or proteins, all detected at peak a

239 FAS ligand neutralization, caspase and GSK-3 inhibitors

240 Although Fas ligand neutralizing antibody could inhibit the forme

241 apoptotic and antiapoptotic molecules (e.g., Fas ligand, Noxa, and Mcl-1).

242 and C3H/He mice and cultured or treated with Fas ligand or acetaminophen after different culture time

243 mediated death but are efficiently killed by Fas ligand or anti-Fas IgM (CH11) upon expression of CD4

244 In contrast to treatment with Fas ligand or gliotoxin, AEA-mediated death was caspase

245 ii) the promotion of T-cell apoptosis by Fas-Fas ligand or granzyme-B pathways, and (iii) their capac

246 etic deletion of the death receptor agonists Fas ligand or TRAIL from the hematopoietic compartment a

247 of Fas-associated death domain, and not Fas, Fas ligand, or caspase proteins, increased following cel

248 monstrated that TNF-alpha, but not perforin, Fas-ligand, or TRAIL, was responsible for bortezomib-sen

249 IL-6, IL-10, IL-12 subunit p70, and soluble Fas ligand (P < 0.01), as well as systemic microvascular

250 d the mRNA expression of CsA-induced p53 and Fas-ligand (P<0.01) and increased that of Bcl-xL, previo

251 is factor-related apoptosis-inducing ligand, Fas ligand, p38alpha mitogen-activated protein kinase, e

252 for expression of the genes caspase 8, Fas, Fas ligand, p53, aggrecanase, matrix metalloproteinase 1

253 induce lung injury via activation of the Fas-Fas ligand pathway and that corticosteroids and GM-CSF r

254 examined expression of components of the Fas-Fas ligand pathway in P. murina-infected mice exposed to

255 ne-based selective pressure, and wherein the Fas ligand pathway was involved in the antitumor respons

256 ted T-lymphocytes impaired OMSCs via the Fas/Fas ligand pathway, as occurs in BMMSCs.

257 ction of B-cell death is not mediated by Fas-Fas ligand pathway, but surprisingly, depends on the up-

258 s of activated T cells by activating the Fas/Fas ligand pathway.

259 aptive immunity, and in the proapoptotic Fas-Fas ligand pathway.

260 ng the perforin/granzyme pathway and not the Fas ligand pathway.

261 is of immature erythroblasts through the Fas-Fas ligand pathway.

262 due to impaired granzyme B/perforin and Fas/Fas ligand pathways and a phenotype of low-intensity chr

263 l (CD4, CD8)-, and immune effector molecule (Fas ligand, perforin)-deficient mice (six mice in each g

264 GE(2) also potentiated apoptosis elicited by Fas ligand plus cycloheximide.

265 Genetic variables (FCGR and Fas/Fas ligand polymorphisms) were examined by 2 degrees of

266 Th17 cells had reduced Fas ligand production and resistance to Fas-induced apop

267 at p65-containing (RelA) complexes bound the Fas ligand promoter and that suppression of activated NF

268 e use of cultured podocytes, expression of a Fas ligand promoter reporter plasmid was higher in HIVAN

269 isplay on their surface an apoptotic form of Fas ligand protein chimeric with streptavidin (SA-FasL)

270 of TNFSF members CD40L, LIGHT, BALM, APRIL, Fas ligand, RANKL, TRAIL-like, and TNF-New in rainbow tr

271 ent to costimulate CD8(+) T cells by driving Fas ligand recruitment into lipid rafts and association

272 Direct confocal microscopy demonstrated that Fas ligand resulted in localized areas of decreased pH a

273 eatment of these melanoma lines with soluble Fas ligand resulted in programmed cell death that was pr

274 ainst death receptor-mediated apoptosis in a Fas ligand-rich environment, such as that of the inflame

275 ory, using mouse models, showed that soluble Fas ligand (sFasL) can efficiently delete donor anti-hos

276 te reaction (MLR) in the presence of soluble Fas ligand (sFasL) to induce AICD in alloreactive cells.

277 ering are applied to a mathematical model of Fas ligand signaling-induced apoptosis.

278 After Fas ligand stimulation, SB-HCV-infected Molt-4 cells had

279 whereas no age-dependent changes in the Fas/Fas ligand system could be detected in human islets.

280 gher nitrotyrosine, malondialdehyde, and Fas/Fas ligand than non-CAD (P<0.05).

281 ysosomes, and colocalizes more strongly with Fas ligand than with CTLA-4, two other molecules that ar

282 lls did not express cytotoxic molecules, but Fas Ligand that can induce Fas-induced apoptosis in targ

283 and produced higher amounts of IFN-gamma and Fas ligand that might contribute to GzmB-independent tum

284 indicated the site of expression of FLIP and Fas ligand [thyroid epithelial cells (TECs) versus infla

285 )-related apoptosis-inducing ligand (TRAIL), Fas ligand, TNF receptor type 2 (TNFR-2), and plasma mic

286 Furthermore, the cytokines Fas ligand, TNF-related apoptosis-inducing ligand, inter

287 Here we show that binding of Fas ligand to Fas activates p38 MAPK in CD8+ T cells and

288 Binding of Fas ligand to Fas mediates activation-induced T cell dea

289 immune attack and up-regulate expression of Fas ligand to promote apoptosis of infiltrating T lympho

290 Secondary lymphoid tissue chemokine and Fas ligand together can attract an array of immune cells

291 In cells exposed to TRAIL or Fas ligand, Top1cc form at the onset of apoptosis.

292 Engagement of Fas by Fas ligand triggers a conformational change that allows

293 ly facilitates the induction of proapoptotic Fas ligand upon TCR restimulation, accounting for enhanc

294 (DC) genetically modified to express IL-4 or Fas ligand was able to reverse established murine arthri

295 s expressing either no FasL or membrane-only Fas ligand were coinjected with L5178Y-R lymphoma cells

296 FLIP and Fas ligand were primarily expressed by TECs in Tg(+) rec

297 ctivity, secreting perforin, granzyme B, and Fas ligand when activated.

298 transforming growth factor-beta, as well as Fas ligand, which inhibits bystander T cell proliferatio

299 unknown how these cells remain resistant to Fas ligand while sensitive to TNF-alpha.

300 ligand/death receptor interactions, such as Fas ligand with Fas, which leads to a caspase activation