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1 ed with the human leukocyte antigen DR4 (HLA-DR4).
2 (-) low HLA-risk siblings (LRS) (non-DR3/non-DR4).
3 RB1*03-DQB1*0201 (DR3) or DRB1*04-DQB1*0302 (DR4)].
4 ltiple sclerosis-associated MHC molecule HLA-DR4.
5 itrullinated alpha-enolase in the context of DR4.
6 lethally irradiated mice transgenic for HLA-DR4.
7 also induced both death receptor (DR)-5 and DR4.
8 f the human T1D susceptibility haplotype HLA-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 entified IA-2 peptides bound to HLA-DR3 and -DR4.
16 ect on cell growth and activation of Fas and DR4.
17 gp-39(263-275) epitope covalently linked to DR4.
18 decreased the enhanced expression of Fas and DR4.
19 cell responses to IA-2 peptides presented by DR4.
20 60 and 853-872 peptides were associated with DR4.
24 15 (found in 36% of subjects), DR3 (in 18%), DR4 (12.5%), DR1 (11%), and DR13 (8%) were associated wi
26 types relevant to T1D, namely, DR3/4, DR3/3, DR4/4, DR3/X, DR4/X, and DRX/X (where X is neither DR3 n
29 hibitor, MS-275, resulted in upregulation of DR4/5 in all GBM cell lines, and these changes could be
30 orters, we show a differential regulation of DR4/5 when exposed to a panel of clinically relevant age
31 expanded T cells from diabetic subjects with DR4, a susceptibility allele for type 1 diabetes, recogn
32 lso abrogated CD437-induced up-regulation of DR4, activation of caspase-8 and caspase-3, and increase
34 Combined treatments comprising the DENV and DR4 affinity-purified fractions of anti-NS1 IgGs (anti-N
35 inhibitory mechanism is bypassed by using a DR4-agonistic antibody that is not subject to this compe
36 that CMFs, engineered to express a specific DR4 allele, can process and present human serum albumin
37 ations post-antibiotic treatment and the HLA-DR4 allele, we generated DR4+/+CD28(-/-)MHCII(-/-) mice,
39 i-CCP antibodies than were those without HLA-DR4 alleles (odds ratio [OR] 5.20, 95% confidence interv
43 ignal-sequence peptides were eluted from HLA-DR4 and -DR3/4 that proved completely identical to a pri
44 g: 1) a cohort enriched in subjects with HLA-DR4 and 2) subjects at risk of RA by virtue of having a
45 rom 39 healthy control subjects selected for DR4 and 23 subjects with recently diagnosed type 1 diabe
47 an interact with TRAIL death receptors (DR), DR4 and DR5 and increase recruitment of FADD and caspase
50 From previous studies the regulation of the DR4 and DR5 cell-death pathways appeared similar; nevert
52 te that regions outside the death domains of DR4 and DR5 have opposite effects to that of Fas in regu
54 mitogen-activated protein kinase leading to DR4 and DR5 induction and resulting in enhancement of th
56 comparison predicted conserved extracellular DR4 and DR5 O-glycosylation sites; progressive mutation
58 gonistic antibodies against TRAIL receptors (DR4 and DR5) are currently being created for clinical ca
59 ession of death receptors (DRs) (TNFR1, Fas, DR4 and DR5) in iPS-derived cardiomyocytes at both prote
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
65 ion promoted ligand-stimulated clustering of DR4 and DR5, which mediated recruitment and activation o
66 tial regulation of the TRAIL death receptors DR4 and DR5--implicating the SRP complex as an essential
76 confirmed demethylation of 5'CpG islands of DR4 and flow cytometry showed an increase in DR4 protein
77 ules (DRAG mice) and those co-expressing HLA-DR4 and HLA-A2 molecules (DRAGA mice) did not differ in
78 e sensitivity of myeloma through DR5 but not DR4 and suggest that a subset of patients with multiple
79 s reveal a previously unappreciated role for DR4 and the extrinsic apoptotic pathway in cell fate cho
81 -)) high HLA-risk siblings (HRS) (DR3 and/or DR4) and AA(-) low HLA-risk siblings (LRS) (non-DR3/non-
82 ough its cognate receptors death receptor 4 (DR4) and death receptor 5 (DR5), preferentially in malig
85 racts with five receptors: death receptor 4 (DR4) and DR5 mediate apoptosis activation, whereas decoy
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
93 eavage, upregulation of Fas-L, Fas, FADD and DR4, and downregulation of bcl-2, phosphorylated bad, bc
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
100 enoids and monoclonal anti-TRAIL receptor-1 (DR4) antibody also induces apoptosis of breast cancer ce
102 lysis identified the TRAIL Death Receptor-4 (DR4) as a potential novel miR-25 target, and this predic
104 , short hairpin RNA silencing of DR5 but not DR4 attenuated TRAIL-mediated lysosomal permeabilization
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
110 mpensates for the weak binding of MBP to HLA-DR4 by maximizing interactions between MS2-3C8 and MBP.
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
121 is expressed on tumor cells, and this TRAIL-DR4 complex is recognized by the TCR through a complemen
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
132 The presence of HLA haplotype DR3-DQ2 or DR4-DQ8 is associated with an increased risk of celiac d
133 6403 children with HLA haplotype DR3-DQ2 or DR4-DQ8 prospectively from birth in the United States, F
136 could distinguish the highest-risk DR4 type (DR4-DQ8) as well as the non-T1D-associated DR4-DQB1*03:0
137 ss likely to carry the highest risk genotype DR4-DQ8/DR3-DQ2 than children with type 1 diabetes from
140 s to pure T cells from either the DQ6 or the DR4/DQ8 mice resulted in significantly different levels
142 ulation analyzed is limited to DR3-DQB1*0201/DR4-DQB1*0302 children with DRB1*0401 (the most common D
144 enhancing diabetes risk among DR3-DQB1*0201/DR4-DQB1*0302 individuals would be alleles of DP and DRB
147 We showed that humanized mice expressing HLA-DR4 (DR0401) molecules and lacking mouse MHC class II mo
149 nd DcR2) co-expressed with death receptor 4 (DR4)/DR5 on the same cell can block the transmission of
153 on of the proapoptotic death receptors (DRs) DR4, DR5, and Fas was not affected by E6 suppression.
155 inant human TRAIL (native TRAIL) and dimeric DR4/DR5 agonist monoclonal antibodies (mAbs) failed in m
157 entrations in combination with TRAIL/agonist DR4/DR5 mAbs in the treatment of TRAIL-resistant tumors.
158 tion of surface TRAIL-receptor 1/receptor 2 (DR4/DR5) levels and to Fas ligand-mediated apoptosis via
159 ation, leading to the induction of Bax, Bim, DR4/DR5, and tumor necrosis factor-related apoptosis-ind
161 rafenib/TRAIL did not increase expression of DR4/DR5, or recruitment of procaspase-8 or FADD to the d
162 E-cadherin bound specifically to ligated DR4/DR5, requiring extracellular cadherin domain 1 and c
167 GAD65 peptides, eluted from HLA-DR3 and -DR4, encompassed two core regions overlapping the two mo
168 easing amounts of peptide in the presence of DR4-expressing antigen-presenting cells to determine fun
169 ing IkappaBalpha protein and thereby induces DR4 expression and subsequent apoptosis in DU145 cells.
170 down of GLI3, but not GLI1 or GLI2, restores DR4 expression and TRAIL sensitivity, indicating that th
175 s sensitivity coincided with upregulation of DR4 expression, while expression of other death effector
177 wing lines of evidence: (a) the p53BS in the DR4 gene is almost identical to the one found in the fir
178 u(9beta), Gln(70beta), and Gln/Arg(74beta)), DR4 (Glu(9beta), Gln/Arg(70beta), and Glu/Ala(74beta)),
180 ociation between serum functionality and HLA-DR4 haplotype and the good response of CU patients to im
181 nsgenic for either A2, A24, B7, DR2, DR3, or DR4 HLA alleles were immunized with overlapping peptides
184 ed or uncitrullinated, were used to immunize DR4-IE-transgenic mice and control mice (class II major
185 hind-ankle swelling (>/=0.3 mm) occurred in DR4-IE-transgenic mice immunized with citrullinated huma
187 urified fractions of anti-NS1 IgGs (anti-NS1-DR4 Ig), but not preimmune control IgGs, in subcytotoxic
189 anti-CCP antibodies are associated with HLA-DR4 in children with polyarticular JRA, whether anti-CCP
190 , we determined the crystal structure of HLA-DR4 in complex with the nonmutated dominant gp100 epitop
193 e of other HLA genotypes without HLA-DR3 or -DR4 in T1DGC new onsets (P = 0.003), and the trend was s
194 ptosis-inducing ligand receptor 1 (TRAIL-R1, DR4), in combination with paclitaxel and carboplatin.
195 as well as a common genetic determinant, HLA-DR4, indicating they may be part of the same disease spe
197 the present study, we have demonstrated that DR4 is a p53 target gene and is regulated by p53 through
198 together, this study provides evidence that DR4 is able to modulate DQ8-restricted T-cell responses,
201 eferences of CD4(+) T cells from several HLA-DR4(+) melanoma patients for different gp100 APLs sugges
203 te as the substrate, with the exception that DR4 mice did not generate detectable amounts of Abs.
205 ngth of vaginal shedding, WT C57BL/6 and HLA-DR4 mice were significantly protected by vaccination.
208 n histocompatibility leukocyte antigen (HLA)-DR4 molecule, and T cell recognition of an epitope of Bo
209 (NOD.RagKO.IL2RgammacKO) mice expressing HLA-DR4 molecules (DRAG mice) and those co-expressing HLA-DR
210 ults demonstrate the importance of human HLA-DR4 molecules in the recognition and presentation of CPA
212 T cells isolated from PBMC obtained from HLA-DR4- normal donors were stimulated ex vivo with autologo
214 = 60 years (58% vs. 23%, P = .004), and HLA DR4 occurred more often in the patients > or = 60 years
215 nfidence interval, 1.1-246; P=0.038) and HLA DR4 (odds ratio, 15.9; 95% confidence interval, 1.07-237
217 Gal-I activity do not affect the function of DR4 or DR5 death receptors upon treatment with TRAIL, im
221 s with either recombinant TRAIL or agonistic DR4- or DR5-specific antibodies has been considered a pr
223 terms of their locations and sequences; (b) DR4 p53BS bound to p53 protein in intact cells upon p53
224 c) a luciferase reporter vector carrying the DR4 p53BS upstream of an SV40 promoter exhibited enhance
225 line having wild-type p53; and (d) when the DR4 p53BS, together with its own corresponding promoter
227 ur common thyroid hormone response elements, DR4, PAL, F2 (LAP), and TSH, and show activities and sel
229 increased anti-CCP antibody formation in HLA-DR4-positive patients with polyarticular-onset JRA.
230 A genetic predisposition to RA, such as HLA-DR4 positivity, indicates that dendritic cells (DC) are
231 t the transcription factor GLI3 binds to the DR4 promoter and Hh requires an intact GLI3-repression a
232 ry effect on signaling through the wild-type DR4 protein can be overcome if the inhibitory mechanism
234 he identification of the novel miR-25 target DR4 provides a mechanism by which miR-25 contributes to
237 en (HA(306-318)) presented by HLA-DR1 or HLA-DR4 represents an ideal system for interrogating pMHC-II
239 Fas-associated death domain, caspase-8, and DR4, respectively, suppressed CD437-induced apoptosis.
240 d a previously identified tumor-reactive HLA-DR4-restricted CD4+ TCR specific for the melanocyte diff
243 d with HLA-DR4, suggesting influences of HLA-DR4-restricted T cells on IA-2-specific B cell responses
244 ivated and sorted CD4(+) T cells can present DR4-restricted type II collagen (CII)-derived peptide in
247 S-ERK-CHOP-mediated up-regulation of DR5 and DR4 signaling, down-regulation of cell survival proteins
248 type (rhTRAIL(WT)) and its death receptor 4 (DR4)-specific variant rhTRAIL(4C7) in human and mouse se
251 2 in type 1 diabetes are associated with HLA-DR4, suggesting influences of HLA-DR4-restricted T cells
253 plus-interleukin-12 (IL-12) vaccination, HLA-DR4 tg animals exhibited robust CPAF-specific IFN-gamma
256 response to Bb antigens with the response of DR4-Tg mice after immunization with Bb outer surface pro
257 ased spirochetal burden as compared with the DR4-Tg mice, as measured by quantitative polymerase chai
260 equency of cirrhosis at presentation and HLA DR4 than patients < or = 30 years, and they have a lower
261 ecules under investigation were HLA-DQ8 and -DR4, the two most prevalent HLA class II alleles found i
262 an directly interact with the TRAIL receptor DR4 thereby preventing Fas-associated death domain recru
263 ts suggest that DR5 may contribute more than DR4 to Apo2L/TRAIL-induced apoptosis in cancer cells tha
265 Furthermore, the Apo2L/TRAIL death receptor DR4 (TRAIL R1) was S nitrosylated following NO-Cbl treat
268 l; then, soluble TRAIL binds to its receptor DR4 (TRAIL-R1), which is expressed on tumor cells, and t
269 inducing signaling cascade complex involving DR4/TRAIL R1, Fas-associated death domain and FLICE-inhi
270 bitors synergized with TRAIL by inducing DRs DR4/TRAIL-R1 and DR5/TRAIL-R2 through NFkappaB activatio
271 indicated a multifactorial effect of the HLA-DR4 transgene on development and function of human CD4 T
272 id Il2rg(-/-) mouse expressing the human HLA-DR4 transgene, infiltration of mouse islets by human T c
273 alleles but express a human HLA allele (HLA-DR4 transgenic [tg] mice) to examine primary immune and
275 es obtained from human MHC II-expressing HLA-DR4 transgenic mice confirmed that 4 of the 5 epitope pe
276 reactive human T cells, 4.13 and 164, in HLA-DR4 transgenic mice on a C57BL/6-derived "diabetes-resis
277 oculation of medroxyprogesterone-treated HLA-DR4 transgenic mice with 5 x 10(5)C. trachomatis D inclu
279 The advantages and limitations of the HLA-DR4 transgenic mouse model for evaluating human C. trach
280 T cell-deficient, superantigen-sensitive HLA-DR4-transgenic (DR4tg) mice, which were compared with th
281 recognition of the 70-kDa autoantigen by HLA-DR4-transgenic mice is focused on a limited number of T
283 clear cells, mouse MAIT hybridoma lines, HLA-DR4-transgenic mice, MAIThighHLA-DR4+ bone marrow chimer
285 -specific TCR were detected in secondary HLA-DR4-transgenic transplant recipients, and these mice wer
286 DR4), and could distinguish the highest-risk DR4 type (DR4-DQ8) as well as the non-T1D-associated DR4
287 and EMSA confirmed that the VDRE at -312 (a DR4-type VDRE) could be bound by vitamin D receptor (VDR
288 7-induced p65 nuclear translocation but also DR4 up-regulation, caspase activation, and DNA fragmenta
293 served that DBA-induced induction of DR5 and DR4 was mediated through generation of reactive oxygen s
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
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