ライフサイエンスコーパス: DR4

1 ed with the human leukocyte antigen DR4 (HLA-DR4).

2 y residues 57-75 (DR1) and residues 182-196 (DR4).

3 (-) low HLA-risk siblings (LRS) (non-DR3/non-DR4).

4 RB1*03-DQB1*0201 (DR3) or DRB1*04-DQB1*0302 (DR4)].

5 ltiple sclerosis-associated MHC molecule HLA-DR4.

6 itrullinated alpha-enolase in the context of DR4.

7 lethally irradiated mice transgenic for HLA-DR4.

8 also induced both death receptor (DR)-5 and DR4.

9 esponse followed by DQ8, DQ0604, DQ0601, and DR4.

10 y Th1 response is induced in the presence of DR4.

11 s of death receptor (DR) 5 but not of Fas or DR4.

12 shed, thus restoring TRAIL signaling through DR4.

13 evaluating the peptide occupancy of DQ8 and DR4.

14 zed the insulin A 1-15 epitope restricted by DR4.

15 f the human T1D susceptibility haplotype HLA-DR4.

16 gp-39(263-275) epitope covalently linked to DR4.

17 entified IA-2 peptides bound to HLA-DR3 and -DR4.

18 ect on cell growth and activation of Fas and DR4.

19 decreased the enhanced expression of Fas and DR4.

20 n presented by the MHC class II molecule HLA-DR4.

21 cell responses to IA-2 peptides presented by DR4.

22 disease since the age of 19 and positive HLA-DR4.

23 60 and 853-872 peptides were associated with DR4.

24 The coexpression of DR4 (0401) diminished DQ8-restricted T-cell responses.

25 g the disease associated HLA-DR3 (0301) and -DR4 (0401) molecules in vitro.

26 Results indicated that DQ8 and DR4 (0401) were able to bind the same hGAD65 peptides.

27 15 (found in 36% of subjects), DR3 (in 18%), DR4 (12.5%), DR1 (11%), and DR13 (8%) were associated wi

28 Among DR4/4 subjects, rs2230199 in C3 was significantly associ

29 types relevant to T1D, namely, DR3/4, DR3/3, DR4/4, DR3/X, DR4/X, and DRX/X (where X is neither DR3 n

30 Utilizing DR4/5 and caspase reporters in parallel, we show that MS

31 of TRAIL (S-TRAIL) by monitoring changes in DR4/5 expression.

32 hibitor, MS-275, resulted in upregulation of DR4/5 in all GBM cell lines, and these changes could be

33 orters, we show a differential regulation of DR4/5 when exposed to a panel of clinically relevant age

34 expanded T cells from diabetic subjects with DR4, a susceptibility allele for type 1 diabetes, recogn

35 lso abrogated CD437-induced up-regulation of DR4, activation of caspase-8 and caspase-3, and increase

36 DR4.AE(o) mice expressed HLA similar to humans and displ

37 Combined treatments comprising the DENV and DR4 affinity-purified fractions of anti-NS1 IgGs (anti-N

38 inhibitory mechanism is bypassed by using a DR4-agonistic antibody that is not subject to this compe

39 that CMFs, engineered to express a specific DR4 allele, can process and present human serum albumin

40 ations post-antibiotic treatment and the HLA-DR4 allele, we generated DR4+/+CD28(-/-)MHCII(-/-) mice,

41 lbumin to a human serum albumin-specific and DR4 allele-restricted T cell hybridoma.

42 i-CCP antibodies than were those without HLA-DR4 alleles (odds ratio [OR] 5.20, 95% confidence interv

43 The HLA B49 and DR4 alleles may increase the risk for recurrence.

44 Women, who have non-DRB1*0401 DR4 alleles more commonly than do men, may respond to a

45 th TRAIL receptors, death receptors 4 and 5 (DR4 and -5).

46 ignal-sequence peptides were eluted from HLA-DR4 and -DR3/4 that proved completely identical to a pri

47 g: 1) a cohort enriched in subjects with HLA-DR4 and 2) subjects at risk of RA by virtue of having a

48 rom 39 healthy control subjects selected for DR4 and 23 subjects with recently diagnosed type 1 diabe

49 eptor (DR)-5 expression but had no effect on DR4 and decoy receptors.

50 tic molecules, including the death receptors DR4 and DR5 as well as Fas and Rip1.

51 Cell surface DR4 and DR5 expression was significantly up-regulated by

52 Rs was independent of p53 because UA induced DR4 and DR5 in HCT116 p53(-/-) cells.

53 mitogen-activated protein kinase leading to DR4 and DR5 induction and resulting in enhancement of th

54 DR4 and DR5 knockdown with siRNA significantly inhibited

55 comparison predicted conserved extracellular DR4 and DR5 O-glycosylation sites; progressive mutation

56 Cell-surface death receptors such as DR4 and DR5 trigger apoptosis through a death-inducing s

57 gonistic antibodies against TRAIL receptors (DR4 and DR5) are currently being created for clinical ca

58 ession of death receptors (DRs) (TNFR1, Fas, DR4 and DR5) in iPS-derived cardiomyocytes at both prote

59 through the O-glycosylated death receptors (DR4 and DR5), but the sensitivity to TRAIL-induced apopt

60 red with normal cells through two receptors (DR4 and DR5).

61 n various cancer cells through its receptors DR4 and DR5, and is currently in clinical trials.

62 ell death through the proapoptotic receptors DR4 and DR5, but the determinants of tumor susceptibilit

63 AIL receptors (TRAIL-R) 1 and 2 (also called DR4 and DR5, respectively) into lipid raft membrane micr

64 ion promoted ligand-stimulated clustering of DR4 and DR5, which mediated recruitment and activation o

65 ive to TRAIL through the two death receptors DR4 and DR5.

66 way through the proapoptotic death receptors DR4 and DR5.

67 rface expression of both the TRAIL receptors DR4 and DR5.

68 ctivates two related proapoptotic receptors, DR4 and DR5.

69 apoptosis-inducing ligand (TRAIL) receptors DR4 and DR5.

70 ability of CD437 to induce the expression of DR4 and DR5.

71 and up-regulate cell surface TRAIL receptors DR4 and DR5.

72 ell death through binding to death receptors DR4 and DR5.

73 impair homo-oligomerization and stability of DR4 and DR5.

74 apoptosis signaling via the death receptors DR4 and DR5.

75 confirmed demethylation of 5'CpG islands of DR4 and flow cytometry showed an increase in DR4 protein

76 ules (DRAG mice) and those co-expressing HLA-DR4 and HLA-A2 molecules (DRAGA mice) did not differ in

77 e sensitivity of myeloma through DR5 but not DR4 and suggest that a subset of patients with multiple

78 s reveal a previously unappreciated role for DR4 and the extrinsic apoptotic pathway in cell fate cho

79 interaction with the death receptors TRAILR1/DR4 and TRAILR2/DR5 in a wide range of cancers, while sp

80 Progression is associated with HLA DR3/DR4 and worsening histological activity.

81 or cell survival advantages through altering DR4 and/or DR5 activity.

82 -)) high HLA-risk siblings (HRS) (DR3 and/or DR4) and AA(-) low HLA-risk siblings (LRS) (non-DR3/non-

83 ough its cognate receptors death receptor 4 (DR4) and death receptor 5 (DR5), preferentially in malig

84 apoptotic genes, including death receptor 4 (DR4) and death receptor 5 (DR5).

85 interaction of TRAIL with death receptor 4 (DR4) and DR5 can trigger apoptotic cell death.

86 biotic treatment is linked to HLA-DRB1*0401 (DR4) and related alleles.

87 by binding to the death receptors TRAIL-R1 (DR4) and TRAIL-R2 (DR5).

88 TRAIL receptor 1/death receptor 4 (TRAIL-R1/DR4) and TRAIL-R2/DR5.

89 DR4/X, and DRX/X (where X is neither DR3 nor DR4), and could distinguish the highest-risk DR4 type (D

90 r the differential genetic susceptibility of DR4+ and DR11+ individuals to the development of chronic

91 g, approximately 94% positive for DR3 and/or DR4, and 29.5% positive for either IA2 or glutamic acid

92 , a myelin-derived self-peptide bound to HLA-DR4, and CD4.

93 eavage, upregulation of Fas-L, Fas, FADD and DR4, and downregulation of bcl-2, phosphorylated bad, bc

94 Rb cells express Fas, DR4, and DR5 on their surfaces, yet were resistant to DR

95 etween humans and mice, is restricted by HLA-DR4, and is a naturally processed self Ag associated wit

96 cells express class II genes and can present DR4- and DQ8-restricted peptides in vitro, suggesting a

97 microscopy using Flag-tagged TRAIL, whereas DR4- and DR5-enhanced green fluorescent protein internal

98 istic human antibody lexatumumab but not the DR4 antibody mapatumumab.

99 Treatment with an antagonistic DR4 antibody or a neutralizing antibody to TRAIL ligand

100 enoids and monoclonal anti-TRAIL receptor-1 (DR4) antibody also induces apoptosis of breast cancer ce

101 Conversely, MS2-3C8 binds MBP-DR4 as tightly as the most avid anti-microbial TCRs.

102 lysis identified the TRAIL Death Receptor-4 (DR4) as a potential novel miR-25 target, and this predic

103 rane and central region constructs were both DR4 associated.

104 , short hairpin RNA silencing of DR5 but not DR4 attenuated TRAIL-mediated lysosomal permeabilization

105 HLA-DR4 binding was confirmed.

106 MBP is loosely accommodated in the HLA-DR4-binding groove, accounting for its low affinity.

107 lines, HLA-DR4-transgenic mice, MAIThighHLA-DR4+ bone marrow chimeras, and humanized NOD-scid IL-2Rg

108 uced expression of death receptor (DR) 5 and DR4 but did not affect expression of decoy receptors in

109 Thus, reexpressing DR4 by 5-AZAdC or retroviral transfection in melanoma ce

110 mpensates for the weak binding of MBP to HLA-DR4 by maximizing interactions between MS2-3C8 and MBP.

111 Hh regulates the expression of DR4 by modulating the activity of its promoter.

112 Knockdown of DR5 and DR4 by small interfering RNA (SiRNA) reduced the sensiti

113 Deletion of DR5 or DR4 by small interfering RNA significantly reduced the a

114 e levels of other related proteins including DR4, c-FLIP, FADD, and caspase-8.

115 Cells expressing the DR4 C336A mutant were more resistant to NO-Cbl and Apo2L

116 NIH-OVCAR-3 cells expressing the DR4 C336A mutation lacked S nitrosylation following NO-C

117 -eight percent of the B burgdorferi-infected DR4+/+CD28(-/-)MHCII(-/-) mice, but none of the B burgdo

118 eatment and the HLA-DR4 allele, we generated DR4+/+CD28(-/-)MHCII(-/-) mice, infected them with Borre

119 steroid therapy, and human leukocyte antigen DR4 characterizes this population.

120 and 25(OH)D at infancy were lower in HLA-DR3/DR4 children among IA case subjects but not in matched c

121 is expressed on tumor cells, and this TRAIL-DR4 complex is recognized by the TCR through a complemen

122 Thus, the MS2-3C8-MBP-DR4 complex reveals the basis for an alternative strateg

123 rated when the immobilized recombinant TRAIL/DR4 complex stimulated the TCR.

124 n upon ligand stimulation, whereas the TRAIL/DR4 complex was not efficiently internalized.

125 ic cells are p53-dependent activation of the DR4 death receptor pathway, caspase 8-mediated cleavage

126 5 transcription and expression; no change in DR4, decoy receptor 1, and decoy receptor 2 expression;

127 us for B and T cell responses to IA-2 in HLA-DR4 diabetic patients that may explain HLA associations

128 s- and ERK-mediated up-regulation of DR5 and DR4, down-regulation of cell survival proteins, and up-r

129 e human leukocyte antigen (HLA) genotype DR3/DR4-DQ8 (HR, 1.35 [95% CI, 1.09-1.68; P = .007]; 10-year

130 children who had the lowest-risk genotypes (DR4-DQ8 heterozygotes or homozygotes).

131 duals who carry the high-risk DR3-DQ2 and/or DR4-DQ8 HLA class II haplotypes.

132 ity and diabetes associated with HLA DR3-DQ2/DR4-DQ8 in U.K. families.

133 The presence of HLA haplotype DR3-DQ2 or DR4-DQ8 is associated with an increased risk of celiac d

134 6403 children with HLA haplotype DR3-DQ2 or DR4-DQ8 prospectively from birth in the United States, F

135 Of 138 informative DR3-DQ2/DR4-DQ8 siblings, 63% shared both haplotypes with their

136 In HLA-identical DR3-DQ2/DR4-DQ8 siblings, the cumulative risk of diabetes by age

137 could distinguish the highest-risk DR4 type (DR4-DQ8) as well as the non-T1D-associated DR4-DQB1*03:0

138 ss likely to carry the highest risk genotype DR4-DQ8/DR3-DQ2 than children with type 1 diabetes from

139 lower responses than the presentation by HLA-DR4/DQ8 APCs.

140 tory cytokine responses as compared with the DR4/DQ8 mice (p < 0.01).

141 s to pure T cells from either the DQ6 or the DR4/DQ8 mice resulted in significantly different levels

142 expressing the neutral DRB1*0402/DQB1*0302 (DR4/DQ8) alleles (p < 0.001).

143 ulation analyzed is limited to DR3-DQB1*0201/DR4-DQB1*0302 children with DRB1*0401 (the most common D

144 We genotyped 457 DR3-DQB1*0201/DR4-DQB1*0302 Diabetes Autoimmunity Study of the Young (

145 enhancing diabetes risk among DR3-DQB1*0201/DR4-DQB1*0302 individuals would be alleles of DP and DRB

146 54108 were associated with DR3-DQB1*0201 and DR4-DQB1*0302.

147 (DR4-DQ8) as well as the non-T1D-associated DR4-DQB1*03:01 type.

148 We showed that humanized mice expressing HLA-DR4 (DR0401) molecules and lacking mouse MHC class II mo

149 In contrast, mice expressing HLA-DR4 (DR0402), HLA-DQ6 (DQ0601), HLA-DQ8 (DQ0302), or HLA

150 nd DcR2) co-expressed with death receptor 4 (DR4)/DR5 on the same cell can block the transmission of

151 performed to investigate the levels of TRAIL DR4, DR5 and OPG receptors generating promising insights

152 TRAIL death receptors (DR4, DR5) are weakly expressed at mRNA, protein, and cel

153 like the other three TRAIL receptors (i.e., DR4, DR5, and DcR1), is regulated by p53.

154 vels, the expression of Fas, p55(TNFR), DR3, DR4, DR5, and DR6 remained largely unchanged.

155 on of the proapoptotic death receptors (DRs) DR4, DR5, and Fas was not affected by E6 suppression.

156 The death receptors (DRs), DR4, DR5, and Fas, transduce cell-extrinsic apoptotic si

157 inant human TRAIL (native TRAIL) and dimeric DR4/DR5 agonist monoclonal antibodies (mAbs) failed in m

158 E-cadherin augmented DR4/DR5 clustering and assembly of the death-inducing si

159 entrations in combination with TRAIL/agonist DR4/DR5 mAbs in the treatment of TRAIL-resistant tumors.

160 tion of surface TRAIL-receptor 1/receptor 2 (DR4/DR5) levels and to Fas ligand-mediated apoptosis via

161 ation, leading to the induction of Bax, Bim, DR4/DR5, and tumor necrosis factor-related apoptosis-ind

162 engagement promoted apoptotic signaling via DR4/DR5, but not Fas.

163 rafenib/TRAIL did not increase expression of DR4/DR5, or recruitment of procaspase-8 or FADD to the d

164 E-cadherin bound specifically to ligated DR4/DR5, requiring extracellular cadherin domain 1 and c

165 lymerization inhibitors similarly attenuated DR4/DR5-induced apoptosis.

166 erin levels displayed greater sensitivity to DR4/DR5-mediated apoptosis.

167 Conversely, EMT attenuated DR4/DR5-mediated DISC formation and caspase-8 stimulatio

168 TCSAVSKGYL (F-EFY) epitope restricted to HLA-DR4, -DR9, and -DR11 (combined allelic frequency: 15% in

169 The heterozygous DR4/DR9 genotype, containing the African-derived "DR9" h

170 GAD65 peptides, eluted from HLA-DR3 and -DR4, encompassed two core regions overlapping the two mo

171 easing amounts of peptide in the presence of DR4-expressing antigen-presenting cells to determine fun

172 ing IkappaBalpha protein and thereby induces DR4 expression and subsequent apoptosis in DU145 cells.

173 down of GLI3, but not GLI1 or GLI2, restores DR4 expression and TRAIL sensitivity, indicating that th

174 IkappaBalpha protein levels and up-regulate DR4 expression in CD437-resistant DU145 cells.

175 tlin-3a and lexatumumab but did not modulate DR4 expression or sensitivity to mapatumumab.

176 lexatumumab efficiency yet did not increase DR4 expression, nor sensitivity to mapatumumab.

177 s sensitivity coincided with upregulation of DR4 expression, while expression of other death effector

178 n intact GLI3-repression activity to silence DR4 expression.

179 wing lines of evidence: (a) the p53BS in the DR4 gene is almost identical to the one found in the fir

180 u(9beta), Gln(70beta), and Gln/Arg(74beta)), DR4 (Glu(9beta), Gln/Arg(70beta), and Glu/Ala(74beta)),

181 Hybridomas were stained with the DR4-gp-39 tetramer and cultured with increasing amounts

182 ociation between serum functionality and HLA-DR4 haplotype and the good response of CU patients to im

183 nsgenic for either A2, A24, B7, DR2, DR3, or DR4 HLA alleles were immunized with overlapping peptides

184 as replaced with the human leukocyte antigen DR4 (HLA-DR4).

185 Mice with HLA-DR3, HLA-DR4, HLA-DQ0601, HLA-DQ0604, or HLA-DQ8 transgenes were

186 ed or uncitrullinated, were used to immunize DR4-IE-transgenic mice and control mice (class II major

187 hind-ankle swelling (>/=0.3 mm) occurred in DR4-IE-transgenic mice immunized with citrullinated huma

188 Treatments with the anti-NS1-DR4 Ig led to plasma leakage, coagulopathy, and morality

189 urified fractions of anti-NS1 IgGs (anti-NS1-DR4 Ig), but not preimmune control IgGs, in subcytotoxic

190 expression of death receptors (DRs) DR5 and DR4 in cancer cells.

191 anti-CCP antibodies are associated with HLA-DR4 in children with polyarticular JRA, whether anti-CCP

192 , we determined the crystal structure of HLA-DR4 in complex with the nonmutated dominant gp100 epitop

193 dds ratio = 30.88), approaching that for DR3/DR4 in European populations.

194 01-transgenic mice to understand the role of DR4 in susceptibility and sex bias in RA.

195 e of other HLA genotypes without HLA-DR3 or -DR4 in T1DGC new onsets (P = 0.003), and the trend was s

196 ptosis-inducing ligand receptor 1 (TRAIL-R1, DR4), in combination with paclitaxel and carboplatin.

197 as well as a common genetic determinant, HLA-DR4, indicating they may be part of the same disease spe

198 These results suggest that DR4-induced endothelial cell sensitization through NS1-e

199 the present study, we have demonstrated that DR4 is a p53 target gene and is regulated by p53 through

200 together, this study provides evidence that DR4 is able to modulate DQ8-restricted T-cell responses,

201 HLA-DR4 is the predominant allele involved in chlamydial ant

202 To further confirm the role of DR4, it was expressed by retroviral vector in SK-MEL-3 a

203 eferences of CD4(+) T cells from several HLA-DR4(+) melanoma patients for different gp100 APLs sugges

204 and hence T cell recognition of gp100 in HLA-DR4(+) melanoma patients.

205 te as the substrate, with the exception that DR4 mice did not generate detectable amounts of Abs.

206 As determined by vaginal shedding, HLA-DR4 mice were more susceptible to a transcervical C. tra

207 ngth of vaginal shedding, WT C57BL/6 and HLA-DR4 mice were significantly protected by vaccination.

208 moral and cellular immune responses than HLA-DR4 mice.

209 Knockdown of DR4 mimics Hh-mediated resistance to TRAIL cytotoxicity.

210 n histocompatibility leukocyte antigen (HLA)-DR4 molecule, and T cell recognition of an epitope of Bo

211 (NOD.RagKO.IL2RgammacKO) mice expressing HLA-DR4 molecules (DRAG mice) and those co-expressing HLA-DR

212 ults demonstrate the importance of human HLA-DR4 molecules in the recognition and presentation of CPA

213 In cells with reactivated DR4, neutralizing mAB to TRAIL reduced apoptosis in resp

214 T cells isolated from PBMC obtained from HLA-DR4- normal donors were stimulated ex vivo with autologo

215 = 60 years (58% vs. 23%, P = .004), and HLA DR4 occurred more often in the patients > or = 60 years

216 nfidence interval, 1.1-246; P=0.038) and HLA DR4 (odds ratio, 15.9; 95% confidence interval, 1.07-237

217 pes have been discovered by elution from HLA-DR4 of pulsed B lymphocytes.

218 Gal-I activity do not affect the function of DR4 or DR5 death receptors upon treatment with TRAIL, im

219 Selective binding to DR4 or DR5 was achieved with three to six-ligand amino a

220 to and trimerizing its functional receptors DR4 or DR5.

221 MHC class II molecules, including HLA-DR1, -DR4, or -DR9.

222 s with either recombinant TRAIL or agonistic DR4- or DR5-specific antibodies has been considered a pr

223 a lower age at diagnosis of disease, as was DR4 (P = 4.67 x 10(-6)) but not DR3.

224 terms of their locations and sequences; (b) DR4 p53BS bound to p53 protein in intact cells upon p53

225 c) a luciferase reporter vector carrying the DR4 p53BS upstream of an SV40 promoter exhibited enhance

226 line having wild-type p53; and (d) when the DR4 p53BS, together with its own corresponding promoter

227 ctivity of a reporter construct with deleted DR4 p53BS.

228 ur common thyroid hormone response elements, DR4, PAL, F2 (LAP), and TSH, and show activities and sel

229 HLA-DR4-positive patients with polyarticular-onset JRA were

230 increased anti-CCP antibody formation in HLA-DR4-positive patients with polyarticular-onset JRA.

231 participants who were HLA-DR3-negative, HLA-DR4-positive, or anti-zinc transporter 8 antibody-negati

232 A genetic predisposition to RA, such as HLA-DR4 positivity, indicates that dendritic cells (DC) are

233 t the transcription factor GLI3 binds to the DR4 promoter and Hh requires an intact GLI3-repression a

234 ry effect on signaling through the wild-type DR4 protein can be overcome if the inhibitory mechanism

235 DR4 and flow cytometry showed an increase in DR4 protein on the cell surface.

236 he identification of the novel miR-25 target DR4 provides a mechanism by which miR-25 contributes to

237 In contrast, DR4 receptor expression was unchanged by Nelfinavir trea

238 TRAIL to induce apoptosis through functional DR4 receptors.

239 en (HA(306-318)) presented by HLA-DR1 or HLA-DR4 represents an ideal system for interrogating pMHC-II

240 Thus, DR4 residue C336 becomes S nitrosylated and promotes apo

241 Fas-associated death domain, caspase-8, and DR4, respectively, suppressed CD437-induced apoptosis.

242 d a previously identified tumor-reactive HLA-DR4-restricted CD4+ TCR specific for the melanocyte diff

243 these mice a valuable model for mapping HLA-DR4-restricted chlamydial epitopes.

244 of the clones recognized previously reported DR4-restricted epitopes within the C-peptide (C25-35) or

245 have been identified as HLA-DR1- and/or HLA-DR4-restricted epitopes.

246 d with HLA-DR4, suggesting influences of HLA-DR4-restricted T cells on IA-2-specific B cell responses

247 ivated and sorted CD4(+) T cells can present DR4-restricted type II collagen (CII)-derived peptide in

248 The DR4-selective Apo2L/TRAIL variants examined in this stud

249 Overexpression of wild-type DR4 sensitized cells to growth inhibition by NO-Cbl.

250 S-ERK-CHOP-mediated up-regulation of DR5 and DR4 signaling, down-regulation of cell survival proteins

251 type (rhTRAIL(WT)) and its death receptor 4 (DR4)-specific variant rhTRAIL(4C7) in human and mouse se

252 tyrosinase and gp100, depending on their HLA-DR4 status.

253 is similar to that of HLA-DRB1*04:02, an HLA-DR4 subtype not associated with RA).

254 2 in type 1 diabetes are associated with HLA-DR4, suggesting influences of HLA-DR4-restricted T cells

255 HLA-DR4 tg and C57BL/6 mice vaccinated with CPAF plus IL-12

256 plus-interleukin-12 (IL-12) vaccination, HLA-DR4 tg animals exhibited robust CPAF-specific IFN-gamma

257 Upon primary bacterial exposure, HLA-DR4 tg mice developed Chlamydia-specific IFN-gamma and a

258 Moreover, C. muridarum-challenged HLA-DR4 tg mice exhibited CPAF-specific antibody and IFN-gam

259 response to Bb antigens with the response of DR4-Tg mice after immunization with Bb outer surface pro

260 ased spirochetal burden as compared with the DR4-Tg mice, as measured by quantitative polymerase chai

261 d anti-Bb antibodies, respectively, than did DR4-Tg mice.

262 interferon-gamma as compared with those from DR4-Tg mice.

263 equency of cirrhosis at presentation and HLA DR4 than patients < or = 30 years, and they have a lower

264 ecules under investigation were HLA-DQ8 and -DR4, the two most prevalent HLA class II alleles found i

265 an directly interact with the TRAIL receptor DR4 thereby preventing Fas-associated death domain recru

266 echanism explaining the modulation effect of DR4 to type 1 diabetes susceptibility.

267 Furthermore, the Apo2L/TRAIL death receptor DR4 (TRAIL R1) was S nitrosylated following NO-Cbl treat

268 DR4 (TRAIL-R1) was identified as one of the genes reacti

269 surface expression of MHC class I, MIC-A/B, DR4 (TRAIL-R1), and Fas (CD95) did not change.

270 l; then, soluble TRAIL binds to its receptor DR4 (TRAIL-R1), which is expressed on tumor cells, and t

271 inducing signaling cascade complex involving DR4/TRAIL R1, Fas-associated death domain and FLICE-inhi

272 bitors synergized with TRAIL by inducing DRs DR4/TRAIL-R1 and DR5/TRAIL-R2 through NFkappaB activatio

273 indicated a multifactorial effect of the HLA-DR4 transgene on development and function of human CD4 T

274 id Il2rg(-/-) mouse expressing the human HLA-DR4 transgene, infiltration of mouse islets by human T c

275 alleles but express a human HLA allele (HLA-DR4 transgenic [tg] mice) to examine primary immune and

276 To assess if HLA-DR4 transgenic and WT mice could be protected by vaccina

277 es obtained from human MHC II-expressing HLA-DR4 transgenic mice confirmed that 4 of the 5 epitope pe

278 reactive human T cells, 4.13 and 164, in HLA-DR4 transgenic mice on a C57BL/6-derived "diabetes-resis

279 oculation of medroxyprogesterone-treated HLA-DR4 transgenic mice with 5 x 10(5)C. trachomatis D inclu

280 suppressor cells (MDSCs) to the liver of HLA-DR4 transgenic mice.

281 The advantages and limitations of the HLA-DR4 transgenic mouse model for evaluating human C. trach

282 T cell-deficient, superantigen-sensitive HLA-DR4-transgenic (DR4tg) mice, which were compared with th

283 recognition of the 70-kDa autoantigen by HLA-DR4-transgenic mice is focused on a limited number of T

284 DR4-transgenic mice were immunized with the HC gp-39 pep

285 clear cells, mouse MAIT hybridoma lines, HLA-DR4-transgenic mice, MAIThighHLA-DR4+ bone marrow chimer

286 identified from 70-kDa/U1-RNA-immunized HLA-DR4-transgenic mice.

287 -specific TCR were detected in secondary HLA-DR4-transgenic transplant recipients, and these mice wer

288 DR4), and could distinguish the highest-risk DR4 type (DR4-DQ8) as well as the non-T1D-associated DR4

289 and EMSA confirmed that the VDRE at -312 (a DR4-type VDRE) could be bound by vitamin D receptor (VDR

290 7-induced p65 nuclear translocation but also DR4 up-regulation, caspase activation, and DNA fragmenta

291 DR4 was associated with IA-2A positivity (P = 5.45 x 10(

292 d to the biotin switch assay; S-nitrosylated DR4 was detected in all three cell lines.

293 n RA patients both negative and positive for DR4 was equal.

294 served that DBA-induced induction of DR5 and DR4 was mediated through generation of reactive oxygen s

295 esidues located in the cytoplasmic domain of DR4 were individually point mutated to alanines.

296 Fas-associated death domain association with DR4, which allows death-inducing signaling complex (DISC

297 2), and peptides were eluted of HLA-DR3 and -DR4, which are associated with highest risk for T1D deve

298 57BL/6-derived mice transgenic for human HLA-DR4 with 70K and either CFA or U1 RNA led to anti-70K an

299 sitive for HLA-DRB1*03 (DR3) or HLA-DRB1*04 (DR4) with DQB1*03:02 (DQ8) have the highest risk of deve

300 to T1D, namely, DR3/4, DR3/3, DR4/4, DR3/X, DR4/X, and DRX/X (where X is neither DR3 nor DR4), and c