ライフサイエンスコーパス: TNFR

1 TNFR expression on mononuclear cells from the dermis and

2 TNFR KO mice showed higher baseline SWS delta power.

3 TNFR levels were unrelated to baseline free TNFalpha lev

4 TNFR superfamily (TNFRSF) members have important immunor

5 TNFR superfamily (TNFRSF)4 (OX40, CD134) and TNFRSF25 ar

6 TNFR-associated death domain protein (TRADD) is a key ef

7 TNFR-associated periodic syndrome (TRAPS, OMIM 142680) i

8 TNFR-specific effects in HF should be considered when th

9 TNFR/TNF superfamily members can control diverse aspects

10 The 55-kDa type 1 TNFR (TNFR1), the key receptor for TNF signaling, is rel

11 bserved in tumor necrosis factor receptor 1 (TNFR-1)(-/-) mice or in wild-type injected with PAI-1-in

12 th baseline levels of plasma TNF receptor-1 (TNFR-1), TNFR-2, and kidney injury molecule-1 (KIM-1) fo

13 ne levels of plasma TNF receptor-1 (TNFR-1), TNFR-2, and kidney injury molecule-1 (KIM-1) for the out

14 In conclusion, TNFR-1, TNFR-2, and KIM-1 independently associated with higher r

15 Associations between doubling in TNFR-1, TNFR-2, and KIM-1 levels and risk of the renal outcomes

16 t baseline, median concentrations of TNFR-1, TNFR-2, and KIM-1 were roughly two-fold higher in the ad

17 nd (TRAIL), Fas ligand, TNF receptor type 2 (TNFR-2), and plasma microparticles--during the earliest

18 h domain adaptor molecule (FADD), caspase-8, TNFR-associated factor 2 (TRAF2), and receptor-interacti

19 not affect hepatotoxic JNK signaling after a TNFR-mediated immune challenge, suggesting specificity i

20 expressing in B lymphocytes both BCL-2 and a TNFR-associated factor 2 (TRAF2) mutant lacking the real

21 9-producing CD4(+) T-helper (TH9) cells in a TNFR-associated factor 6 (TRAF6)- and NF-kappaB-dependen

22 CD27 is a TNFR family member expressed on T cells, and its ligand,

23 -FMK also induced Rip1-phosphorylation via a TNFR-independent mechanism.

24 hrough its interactions with tubulin, actin, TNFR-associated factor-3 (Traf3), IL-13R1, and DISC1.

25 signaling complex that contained the adapter TNFR-associated factor 2 as well as PKB and its upstream

26 The signaling adaptor TNFR-associated factor 1 (TRAF1) is specifically lost fr

27 Rs not only have implications for additional TNFR family members, but also provide potential targets

28 une mediators/regulators linked to TNF-alpha/TNFR signaling, nuclear factor kappa-B (NF-kappaB) activ

29 lant rejection that is exclusively TNF-alpha/TNFR-dependent.

30 Two counterregulatory molecules, TNF-alphaR (TNFR) 1 and TNFR2, modulate the pathological effects of

31 itment of receptor interacting protein 1 and TNFR-associated factor 2 to the DR3 signaling complex an

32 TBK1, TGF-beta-activated kinase (TAK) 1, and TNFR-associated factor 6, whereas not affecting p65-indu

33 IKKepsilon, TNFR-associated factor 2, and TNFR-associated factor 5 were also required to mediate t

34 in global sleep architecture in C57BL/6J and TNFR KO mice.

35 ted with TNF-alpha neutralizing antibody and TNFR KO mice showed increased EEG SWS activity.

36 the residual cytolytic activity is CD95 and TNFR dependent.

37 ed on TNF production by BM-derived cells and TNFR expression by radioresistant IECs.

38 the population of highly injected cells, and TNFR-deficient mice displayed enhanced susceptibility to

39 sis factor receptors (TNFRs): Fas, FasL, and TNFR superfamily member 1B.

40 naling through its interaction with NEMO and TNFR-associated factor 2.

41 ctivated kinase 1 (TAK1) phosphorylation and TNFR-associated factor (TRAF) 6 ubiquitination in BMMCs

42 ereas MyD88, Toll/IL-1R adaptor protein, and TNFR-alpha-associated factor 6 recruitments to TLR2 were

43 -family adapter proteins involved in TLR and TNFR pathways.

44 Our results reveal that a prototypic TLR and TNFR signaling pathway is used by a killer cell Ig-like

45 se, IRAK1, TLR1, TLR4, TLR6, TLR8, TLR9, and TNFR-associated factor 6) were downregulated, whereas an

46 rofound ramifications for the use of TNF and TNFR antagonists in human SLE and related autoimmune dis

47 ptors, including those of the Notch, Wnt and TNFR/IKK/NF-kappaB pathways, and discuss the potential r

48 II, but not the interaction between PGRN and TNFRs.

49 l or functional interaction between PGRN and TNFRs.

50 ow demonstrate that different agonistic anti-TNFR antibodies have specific requirements for FcgammaRI

51 optimal biological effects of agonistic anti-TNFR antibodies.

52 ign of more potent antitumor agonistic, anti-TNFR therapies, the underlying mechanism has remained ob

53 (RAG) knockout (KO) (no T or B cells)-based TNFR double and triple KO mice were generated.

54 Because TNFR-associated factor 6 (TRAF6) has been reported to be

55 domain-containing adaptor inducing IFN-beta/ TNFR-associated factor 3 pathway was highly upregulated

56 However, cell death protection through both TNFR was mediated through the Bcl-2/Bcl-xL pathway.

57 l can be mediated independently through both TNFR.

58 arcinogenesis that was partially mediated by TNFR signaling, indicating that TAK1 is an essential com

59 mitochondrial depolarization is mediated by TNFR-associated factor-1 (TRAF-1) and TRAF-2 degradation

60 LR families, whose signals are transduced by TNFR-associated factor (TRAF) molecules.

61 mice expressing the mitochondrial chaperone TNFR-associated protein 1 (TRAP1) in the prostate develo

62 Using an established system of chimeric TNFRs and novel ligand variants mimicking the bioactivit

63 sion, elevated concentrations of circulating TNFRs in patients with type 2 diabetes at baseline are v

64 In conclusion, TNFR-1, TNFR-2, and KIM-1 independently associated with

65 We identified a conserved TNFR-associated factor 6 (TRAF6) binding motif, which wa

66 n this study, we show that the costimulatory TNFR CD27 provides a dual trigger that can enhance survi

67 The costimulatory TNFR family member GITR can provide important survival s

68 treatment with the cTfRMAb-GDNF and cTfRMAb-TNFR fusion proteins caused a significant 54%, 69% and 3

69 or (d) the combined cTfRMAb-GDNF and cTfRMAb-TNFR fusion proteins, following a 1-h reversible middle

70 eins are designated cTfRMAb-GDNF and cTfRMAb-TNFR, respectively.

71 nflammatory therapies based on soluble decoy TNFRs.

72 t oxidative stress enhanced ligand-dependent TNFR signaling.

73 tions in vitro to limit caspase-8-dependent, TNFR-induced apoptosis, and animals lacking RIPK1, RIPK3

74 erated potent agonists against two different TNFR superfamily receptors and mouse tumor model studies

75 for JNK restraint activated during distinct TNFR-mediated challenges.

76 velopment and highlight the role of distinct TNFRs in initial and terminal differentiation stages in

77 diate p75(NTR) signaling are trimeric (i.e., TNFR-associated factor 6 or TRAF6).

78 h receptors nor the classical MAVS effectors TNFR-associated factor-2, IRF-3/7, or IFN-beta but the p

79 linical profiles of mice deficient in either TNFR alone did not differ from those in each other or fr

80 nsistent with the hypothesis that epithelial TNFR signaling participates in mucosal healing.

81 These encouraging data establish TNFRs as important targets for enhancing tumor-specific

82 not colonic epithelial cells (CECs), express TNFRs were also generated.

83 perfamily member 15 (TL1A) is the ligand for TNFR superfamily (TNFRSF)25.

84 ization and clustering is a prerequisite for TNFR intracellular signaling, and as m4-1BBL can only re

85 s were incubated with conditioned media from TNFR-costimulated T lymphocytes, and type I collagen exp

86 ive and argue for the use of next-generation TNFR-selective TNF therapeutics as an effective approach

87 atment with BBB penetrating IgG-GDNF and IgG-TNFR fusion proteins enhances the therapeutic effect of

88 ese effects are mediated through the type II TNFR (TNFR2).

89 IKKepsilon, TNFR-associated factor 2, and TNFR-associated factor 5 w

90 ies of antibodies targeting immunoregulatory TNFRs expressed by T cells.

91 mation over 3 days; hgd40 reduced colitis in TNFR double-knockout mice.

92 Associations between doubling in TNFR-1, TNFR-2, and KIM-1 levels and risk of the renal o

93 Further, in TNFR(-/-) mice, neutrophils accumulated normally in resp

94 d SCN activation in control mice, but not in TNFR-1 mutants.

95 r 2 (TRAF2), suggesting a regulatory role in TNFR signaling.

96 decreased in C57BL/6J, and was unaffected in TNFR KO mice as well as in C57BL/6J mice exposed to SF b

97 her this effect segregates at the individual TNFR.

98 Glucocorticoid-induced TNFR (Gitr) and Ox40, two members of the TNFR superfamil

99 her anti-CD25 or anti-glucocorticoid-induced TNFR exacerbated intestinal pathology, and, in addition,

100 n, CTLA-4 exon 2, and glucocorticoid-induced TNFR exon 5, were phenotypically unstable, and exhibited

101 t by upregulating the glucocorticoid-induced TNFR family-related protein (GITR) and increasing GITR s

102 Glucocorticoid-induced TNFR family-related protein (GITR)-mediated activation o

103 n has shown that anti-glucocorticoid-induced TNFR family-related protein agonistic Ab DTA-1 (rat or m

104 receptor binding and glucocorticoid-induced TNFR family-related protein-induced T cell agonistic pro

105 h a stimulatory Ab to glucocorticoid-induced TNFR family-related receptor (GITR) has previously been

106 icant upregulation of glucocorticoid-induced TNFR family-related receptor on conventional T cells dur

107 a their expression of glucocorticoid-induced TNFR ligand.

108 ice treated with anti-glucocorticoid-induced TNFR were able to expel worms more rapidly, implying the

109 her, T cell-intrinsic glucocorticoid-induced TNFR-related protein (GITR) contributes to 4-1BB express

110 Glucocorticoid-induced TNFR-related protein (GITR) is a costimulatory molecule

111 se targeting OX40 and glucocorticoid-induced TNFR-related protein (GITR).

112 levated expression of glucocorticoid-induced TNFR-related protein (GITR).

113 es targeting the TNFR glucocorticoid-induced TNFR-related protein (GITR; TNFRSF18; CD357) expressed o

114 CD27, TNFR2 p75, and glucocorticoid-induced TNFR-related protein compared with transferred CD28(+/+)

115 Agonistic antibodies to apoptosis-inducing TNFRs, such as death receptor 5 (DR5), although displayi

116 We investigated TNFR expression in clinical samples and function in shor

117 y transplants were performed using MIEP-lacZ TNFR DKO or MIEP-lacZ TNFRwild-type donor mice.

118 ifs found in the cytoplasmic domains of many TNFR family members and their adaptor proteins may serve

119 wever, PG102 stimulated normal CD40-mediated TNFR-associated factor (TRAF)2 and TRAF3 degradation.

120 6J and in TNF-alpha double receptor KO mice (TNFR KO).

121 vivo, and treatment with the small molecule TNFR inhibitor R-7050 partially protected hyperoxaluric

122 Rs extended to an antibody targeting the non-TNFR receptor CTLA-4 (CD152) that acts as a negative reg

123 nvolves hemopoietic cross-talk, and numerous TNFR superfamily members have been implicated in this pr

124 tly can augment the anti-tumor activities of TNFR antibodies by enhancing their agonistic activities

125 nsequently, generating effective agonists of TNFR superfamily receptors is challenging.

126 and themselves, and regulate the assembly of TNFR signalling complexes.

127 Furthermore, therapeutic blockade of TNFR might delay progressive forms of nephrocalcinosis i

128 At baseline, median concentrations of TNFR-1, TNFR-2, and KIM-1 were roughly two-fold higher i

129 of osteoclastogenesis and for degradation of TNFR-associated factor 6 in osteoclast precursors.

130 usly found that T cell-intrinsic deletion of TNFR-associated factor (TRAF) 6 (TRAF6DeltaT) in mice re

131 he signal transduction network downstream of TNFR and upstream of IKK, and depends on the level of th

132 Expression of TNFR and IL-6 in the dermis was reversible in a patient

133 ogenic activities by retaining expression of TNFR-1 and -2 and VEGF receptor 2 in ECs.

134 CHQ elevated expression of TNFR-associated factor 6, a common intermediate in IL-1R

135 R2, we demonstrate differential functions of TNFR in human monocyte-derived and blood CD1c(+) DC.

136 L-1R-associated kinase 1, but independent of TNFR-associated factor 6.

137 Inhibition of TNFR signaling prevented the induced expression of the c

138 Knockdown of TNFR-associated factor 6 or NF-kappaB activator 1 in 70Z

139 indings demonstrate that PGRN is a ligand of TNFR, an antagonist of TNFalpha signaling, and plays a c

140 It also suggests that TRAF6, a mediator of TNFR and TLR signaling, may be a common signaling interm

141 uce the freely available cytoplasmic pool of TNFR-associated factor (TRAF)2 and cellular inhibitors o

142 ling and Nfkbie, and a negative regulator of TNFR signal transduction.

143 nalysis were used to investigate the role of TNFR signaling in the early intragraft activation of cel

144 In this study, we examined the role of TNFR-associated factor (TRAF)4 in IL-17 signaling and Th

145 ] is an essential kinase linking a subset of TNFR family members to the noncanonical NF-kappaB pathwa

146 40 and mediates K63-linked ubiquitination of TNFR-associated factor3 (TRAF3).

147 that are best known as signaling adapters of TNFRs.

148 Concentrations of TNFRs moderately associated with death unrelated to ESRD

149 While the extracellular domains of TNFRs form trimeric complexes with their ligands and the

150 ovide evidence for a stepwise involvement of TNFRs in mTEC development, with CD40 upregulation induce

151 ecruitment of PKB and PI3K were dependent on TNFR-associated factor 2 and on translocation of OX40 in

152 kappaB activation by beta(c) is dependent on TNFR-associated factor 6 (TRAF6) and that association of

153 We now show that one TNFR family member, OX40 (CD134), after ligation by OX40

154 iR-146a targets IL-1R-associated kinase 1 or TNFR-associated factor 6, suggesting the regulatory effe

155 iated immune cell responses in TNF-alpha- or TNFR-deficient mice.

156 e received TNFR 1 (p55) knockout (KO) and/or TNFR 2 (p75) KO donor T cells.

157 n of engineered antibodies to OX40 and other TNFR with improved anti-tumor activity.

158 yer in controlling the availability of other TNFR family members.

159 Analysis of other TNFR sequences suggests proline-containing sequences as

160 In contrast to other TNFR agonists, such as anti-4-1BB, which can cause immun

161 Similar to other TNFR ligands, CD70 has been shown to initiate intracellu

162 Mice solely lacking parenchymal TNFRs (C57 --> TNFRsf1a/1b(-/-)) had milder disease than

163 , raising the possibility that aberrant PGRN-TNFR interactions underlie the molecular basis for neuro

164 sative agent of smallpox, is the most potent TNFR of those tested here including hTNFR2.

165 with the soluble recombinant fusion protein TNFR:Fc slowed disease progression in UmodC147W/+ mice b

166 The cytoplasmic adaptor proteins TNFR-associated factor (TRAF)3 and TRAF6 are important m

167 sequently, in the absence of c-IAP proteins, TNFR-mediated activation of NF-kappaB and MAPK pathways

168 e (1 mum) that was not sufficient to provoke TNFR self-association resulted in increased TNF-induced

169 eby limiting crosstalk between ITAM and RANK/TNFR signaling and allowing fine tuning of osteoclastoge

170 cells in a signal 3 manner, F1 mice received TNFR 1 (p55) knockout (KO) and/or TNFR 2 (p75) KO donor

171 peripheral glia, and the TNF-alpha receptor (TNFR), Wengen, is expressed in motoneurons.

172 ptor (TLR) and TNF-family cytokine receptor (TNFR) signaling pathways.

173 deletion of tumor necrosis factor receptor (TNFR) 1 and TNFR2 (TNFR double knockouts); some mice wer

174 xpression of tumor necrosis factor receptor (TNFR) 2 is induced in situ by ischemia/reperfusion injur

175 ction of the tumor necrosis factor receptor (TNFR) CD27 with its ligand CD70 is an emerging target to

176 the type II tumor necrosis factor receptor (TNFR) decoy receptor.

177 that target tumor necrosis factor receptor (TNFR) family members have shown dependence on expression

178 mbers of the tumor necrosis factor receptor (TNFR) family with agonist Abs enhances T cell function,

179 Tumor necrosis factor receptor (TNFR) preligand assembly domain (PLAD) has been found to

180 nging to the tumor necrosis factor receptor (TNFR) superfamily are emerging as promising cancer immun

181 sponses, the tumor necrosis factor receptor (TNFR) superfamily members have emerged as attractive tar

182 a member of tumour necrosis factor receptor (TNFR) superfamily, has a pivotal role in B-cell-mediated

183 mber of the tumour necrosis factor receptor (TNFR) superfamily, has the capacity to cause extensive a

184 ember of the tumor necrosis factor receptor (TNFR) superfamily, is expressed on antigen-presenting ce

185 ember of the tumor necrosis factor receptor (TNFR) superfamily, whose members undergo trimeric oligom

186 eptor in the tumor necrosis factor receptor (TNFR) superfamily.

187 tor (TLR)-2, tumor necrosis factor receptor (TNFR)-1 and closely related NOD1, all of which share com

188 Ablation of tumour necrosis factor receptor (TNFR)-1/-2, Myeloid Differentiation primary response gen

189 Tumor necrosis factor receptor (TNFR)-associated factor 2 (TRAF2) and TRAF5 are adapter

190 Tumor necrosis factor receptor (TNFR)-associated factor 2 (TRAF2) is a pivotal intracell

191 pter protein tumor necrosis factor receptor (TNFR)-associated factor 3 (TRAF3) is both modified by an

192 Tumor necrosis factor receptor (TNFR)-associated factor 6 (TRAF6) is an adapter protein

193 Tumor necrosis factor receptor (TNFR)-associated factor 6 (TRAF6) is an important adapto

194 Tumor necrosis factor receptor (TNFR)-associated factors (TRAFs) form a family of protei

195 ogy with the tumor-necrosis-factor receptor (TNFR)-associated factors TRAF2 and TRAF3.

196 Tumor necrosis factor receptor (TNFR)-associated periodic syndrome (TRAPS) is an autosom

197 coid-induced tumor necrosis factor receptor (TNFR)-related protein (GITR) elicits antitumor activity

198 actor in the tumor necrosis factor-receptor (TNFR) and Toll-like receptor (TLR) pathways.

199 urther analysis, antibodies to TNF receptor (TNFR) 1 or 2 were applied, or CSD was monitored in TNFR1

200 Selective inhibition of TNF receptor (TNFR) 1 signaling holds the potential to greatly reduce

201 use of the differential use of TNF receptor (TNFR) family costimulatory receptors.

202 The role of intragraft TNF receptor (TNFR) signaling in activation of gene expression in allo

203 Individual TNF receptor (TNFR) signaling in RBR was evaluated in BM-EPCs from WT,

204 ptosis, processes that involve TNF receptor (TNFR) signaling.

205 costimulatory molecules in the TNF receptor (TNFR) superfamily are viewed as a major source of this s

206 Agonistic anti-TNF receptor (TNFR) superfamily member antibodies are a class of promi

207 LMP1 functionally mimics TNF receptor (TNFR) superfamily member CD40, but LMP1 signals and down

208 eptor 3 (DR3), a member of the TNF receptor (TNFR) superfamily, is induced in human renal tubular epi

209 ath receptors, a subset of the TNF receptor (TNFR) superfamily.

210 ingly suppressed expression of TNF receptor (TNFR)-1 and -2, decreased TNF-alpha-induced phosphorylat

211 o investigate the influence of TNF receptor (TNFR)-costimulated lymphocytes on collagen expression in

212 of the tumor-necrosis factor (TNF) receptor (TNFR)-associated factor (TRAF) family in T cell immunity

213 rs of tumour necrosis factor (TNF) receptor (TNFR)-mediated signalling.

214 eling responses in HF that are TNF-receptor (TNFR) specific.

215 r necrosis factor alpha (TNFalpha) receptor (TNFR) families] help drive and control intestinal inflam

216 osis factor receptor/interleukin-1 receptor, TNFR/IL-1R in mammals) is indispensable for intestinal i

217 en PGRN and tumor necrosis factor receptors (TNFR I/II) was reported and proposed to be a mechanism b

218 antithetic effects of the two TNF receptors (TNFR) in the central nervous system, whereby TNFR1 has b

219 the precise role of the TNF-alpha receptors (TNFRs) has not been well defined using in vivo models.

220 TNF signals via two distinct receptors (TNFRs).

221 directly to tumor necrosis factor receptors (TNFRs) and disturbed the TNFalpha-TNFR interaction.

222 e family of tumor necrosis factor receptors (TNFRs) and their ligands form a regulatory signaling net

223 in-13 and 3 tumor necrosis factor receptors (TNFRs): Fas, FasL, and TNFR superfamily member 1B.

224 stem is to encode homologs of TNF receptors (TNFRs) that block TNF-alpha function.

225 ocytosed CD137-containing vesicles recruited TNFR-associated factor (TRAF) 2 and were decorated with

226 Although the TNFR family recruits TNFR-associated factor (TRAF) molecules leading to IKKal

227 STING recruits TNFR-associated NF-kappaB kinase-binding kinase 1 which

228 nt of cylindromatosis coincided with reduced TNFR-associated factor 6 autoubiquitination and lower NF

229 signaling among the therapeutically relevant TNFR superfamily of receptors.

230 In addition to its proinflammatory role, TNFR signaling induces expression of SOCS3, a negative r

231 of three PGRN fragments, exhibited selective TNFR binding.

232 with neutralizing anti-TNF-alpha Ab, soluble TNFR, or an inhibitor of NF-kappaB, or by attenuating th

233 Levels of these soluble TNFRs (sTNFRs) are reported to be elevated in children w

234 ve impaired signaling downstream of specific TNFR family members such as 4-1BB.

235 biquitin:NIK E3 ligase comprised of subunits TNFR-associated factors (TRAF)3, TRAF2, and cellular inh

236 T cells transfected with CFP- and YFP-tagged TNFRs exposed to the thiol oxidant diamide.

237 We conclude that TNFR signaling is essential for CaOx crystal adhesion to

238 We recently reported that TNFR-associated factor (TRAF)3, a ubiquitously expressed

239 Here, we tested the hypothesis that TNFRs also have a direct role in tubular crystal deposit

240 The TNFR family member 4-1BB plays a key role in the surviva

241 The TNFR family member OX40 (CD134) is critical for optimal

242 The TNFR-associated factor (TRAF) proteins have a vital role

243 The TNFR-associated factor (TRAF)2 and TRAF6 adaptor protein

244 formation of a DISC involving TNF-alpha, the TNFR-associated death domain adaptor molecule (TRADD), t

245 Although the TNFR family recruits TNFR-associated factor (TRAF) molec

246 Both the GDNF and the TNFR are large molecules that do not cross the blood-bra

247 The GDNF and the TNFR decoy receptor were re-engineered for BBB transport

248 gulation of signaling by members of both the TNFR superfamily and innate immune receptors.

249 ation of NF-kappaB signaling pathways by the TNFR: TNFR1 activated both the p65 and p52 pathways, whe

250 mune cells from knock-in mice expressing the TNFR-associated factor 6 (TRAF6) binding-defective mutan

251 Having previously described a role for the TNFR superfamily member CD27, we since screened for othe

252 eceptor 3 (DcR3) is a soluble protein in the TNFR superfamily.

253 important adaptor molecule that mediates the TNFR family and interleukin-1 (IL-1)/Toll-like receptor

254 ducibly express a number of receptors of the TNFR and TLR families, whose signals are transduced by T

255 We found that 4-1BB (CD137), a member of the TNFR family, together with CD103, marked mesenteric lymp

256 Death receptors (DRs) of the TNFR superfamily contribute to antiviral immunity by pro

257 OX40 is a member of the TNFR superfamily that has potent costimulatory propertie

258 CD27, a member of the TNFR superfamily, is constitutively expressed in most T

259 Decoy receptor 3 (DcR3), a member of the TNFR superfamily, is overexpressed in tumor cells and is

260 ced TNFR (Gitr) and Ox40, two members of the TNFR superfamily, play important roles in regulating act

261 from an agonist Ab to 4-1BB, a member of the TNFR superfamily, results in detrimental effects on immu

262 erate agonistic Abs targeting members of the TNFR superfamily, such as OX40, 4-1BB, and GITR, express

263 gulatory functions, including members of the TNFR superfamily, the Toll-like receptor (TLR) family, t

264 se gene Pla2g7 and Tnfrsf21, a member of the TNFR superfamily.

265 signaling from OX40 (CD134), a member of the TNFR superfamily.

266 A20--an inducible feedback inhibitor of the TNFR, RIG-I, and TLR signaling pathways that broadly con

267 IgG fusion proteins, wherein the GDNF or the TNFR are fused to the heavy chain of a chimeric monoclon

268 ntitumor effects of antibodies targeting the TNFR glucocorticoid-induced TNFR-related protein (GITR;

269 We recently demonstrated that the TNFR family costimulatory molecule OX40 (CD134) is criti

270 of TNF production to models of the TLR-, the TNFR-, and the NFkappaB signaling modules, we were able

271 mbining anti-PD-L1 with agonistic Abs to the TNFR superfamily members, OX40 and CD27.

272 l costimulatory molecule that belongs to the TNFR superfamily.

273 ongly replicating (i.e., virulent) VACV, the TNFR family costimulatory receptors OX40 (also known as

274 The TNFRs play a critical role in activating intragraft expr

275 nse and the complex interactions between the TNFRs and other cytokine signaling pathways in the early

276 stent with an allosteric modification of the TNFRs.

277 eview will focus on agonists that target the TNFRs OX40, 4-1BB, and CD40.

278 This highlights a quantitative role of this TNFR family second signal to supplement signal 1.

279 rther underlining the key importance of this TNFR superfamily member in regulation of thymic microenv

280 s unclear which cell types activated through TNFR-associated signaling cascades are involved in the p

281 lencing AC7, changes in mRNA levels of TLR1, TNFR-associated factor 6, and ST2 were seen and unchange

282 s factor-tumor necrosis factor receptor (TNF-TNFR) pairs have provided the first logical, hypothesis-

283 D alone and together increase levels of TNF/TNFR family members and NF-kappaB-regulated genes.

284 cognate receptor Fn14 are members of the TNF/TNFR superfamily and are upregulated in tumors.

285 receptors (TNFRs) and disturbed the TNFalpha-TNFR interaction.

286 In TNF-treated cells, TNFR1, TNFR-associated death domain protein (TRADD), Fas-associ

287 necrosis factor receptor (TNFR) 1 and TNFR2 (TNFR double knockouts); some mice were given a GATA3-spe

288 ns for the design of agonistic antibodies to TNFR as therapeutics.

289 viously reported that PGRN directly binds to TNFR and significantly enhances Treg population and stim

290 at upon macrophage stimulation, p62 binds to TNFR-associated factor 6, another E3 ligase important fo

291 ich IL-10 can suppress cellular responses to TNFR family members.

292 not result in an increase in TNF binding to TNFRs, it resulted in increased TNF-induced activation o

293 survival factor for DC, the role of the two TNFR, TNFR1 and TNFR2, in mediating these effects is poo

294 Thus, the stalk regions of the two TNFRs not only have implications for additional TNFR fam

295 dylic acid-induced formation of the upstream TNFR-associated factor (TRAF) 3/TANK-binding kinase (TBK

296 CD40 and LMP1 both use TNFR-associated factor (TRAF) adaptor proteins, but in d

297 Whereas TNFR-induced RIPK3-dependent necroptosis requires RIPK1,

298 study was undertaken to investigate whether TNFR PLAD limits inflammatory skin injury in a mouse mod

299 ed with CD3/CD28 beads and costimulated with TNFR-selective variants.

300 Although it is normally linked with TNFR signaling pathways, TRAF5 constitutively associated