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 cytotoxic (IFNgamma, granzyme B, perforin-1, Fas ligand) and apoptotic (cleaved caspase-3) effector m

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

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

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

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

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

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

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

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

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

47 Transcripts of Fas ligand are abnormally increased in autoimmune hepati

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

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

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

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

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

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

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

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

56 B-lymphoblasts with significant increase in Fas Ligand (CD95L) (FasL), CD69, and IL-R1 expression, a

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

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

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

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

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

62 FAS ligand deficiency should be screened in patients pre

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 2,4-dinitro-1-fluorobenzene (DNFB) required Fas ligand (FasL) and perforin expression.

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

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

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

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

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

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

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

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

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

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

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

107 Fas ligand (FasL) causes apoptosis of epidermal keratino

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

109 Fas ligand (FasL) exerts potent proapoptotic and proinfl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

129 Fas ligand (FasL) is one potential target.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

175 when the MBP-specific CD8+ T cells expressed Fas ligand (FasL).

176 negatively regulate autoreactive B cells via Fas ligand (FasL).

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

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

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

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

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

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

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

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

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

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

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

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

189 CXCL10, fatty acid binding protein (FABP) 2, fas ligand (FASLG), matrix metalloproteinase (MMP) 1, MM

190 FAS ligand function was assessed based on reactivation-i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

219 For example, Fas ligand is commonly overexpressed in TMEs and induces

220 Fas ligand is one such molecule whose cell surface expre

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

238 FAS ligand neutralization, caspase and GSK-3 inhibitors

239 Although Fas ligand neutralizing antibody could inhibit the forme

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

261 cell death through perforin-granzyme and Fas-Fas ligand pathways(3,4).

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

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

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

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

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

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

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

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

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

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

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

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

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

275 interleukin 10 (IL-10) and IL-18 and soluble FAS ligand (sFASL) were measured by enzyme-linked immuno

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

291 5 in response to GEM sensitised the cells to fas ligand treatment, was associated with increased phos

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 rative syndrome, and had impaired TCR-driven Fas ligand upregulation, providing a mechanism for the T

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

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