ライフサイエンスコーパス: HLA

1 HLA matching had a statistically significant impact on g

2 HLA typing was performed for 449 participants.

3 HLA-B*46 (one of the commonest HLA class I alleles in SE

4 HLA-DQ mismatch is a significant risk factor for de novo

5 HLA-DQ-gluten tetramers can be used to detect gluten-spe

6 HLA-DR15 and HLA-DR1 exhibit distinct peptide repertoire

7 HLA-DR15(+) and HLA-DR1(+) healthy human donors display

8 HLA-DR15-alpha3135-145 tetramer(+) T cells in HLA-DR15 t

9 HLA-DR7 was present in 88% compared to 19.6% in healthy

10 ith AML who underwent HCT from 9/10 or 10/10 HLA-matched unrelated donors.

11 Remarkably, 32% of 113 HLA-B8, 34% of 98 HLA-B12, and 9% of 66 HLA-B35 donors s

12 CT recipients, including 125 cord blood, 125 HLA-mismatched, and 154 HLA-matched HCTs, detection of m

13 125 cord blood, 125 HLA-mismatched, and 154 HLA-matched HCTs, detection of multiple viruses was comm

14 113 HLA-B8, 34% of 98 HLA-B12, and 9% of 66 HLA-B35 donors showed platelet antigen expression that w

15 k loci including previously identified 6p21 (HLA-DRA and DPB1), 17q12 (ORMDL3), 3q13.33 (CD80), 2q32.

16 eive myeloablative HCT from an available 8/8-HLA matched URD.

17 ve with T1D were enrolled if they had 1 of 9 HLA genotypes associated with a risk for T1D.

18 Remarkably, 32% of 113 HLA-B8, 34% of 98 HLA-B12, and 9% of 66 HLA-B35 donors showed platelet ant

19 , and cytokine production was inhibited by a HLA-DR blocking Ab.

20 tion and transplantation of a kidney from an HLA-incompatible donor.

21 fore the transplantation of a kidney from an HLA-incompatible donor.

22 V)-infected HLA-A2(-) individual received an HLA-A2(+) liver allograft.

23 We investigated whether an HLA-DQ-gluten tetramer-based assay accurately identifies

24 ion of the antigen serotypes HLA-A*02:01 and HLA-B*27:05 expressed on the Epstein-Barr virus-transfor

25 MUC4, MUC6, MUC2, SIRPA, HLA-DRB1, HLA-A and HLA-B molecules.

26 (lower resolution) HLA typing for HLA-A and HLA-B, and allele-level for HLA-DRB1.

27 )H3.3K27M(+) glioma cells in an antigen- and HLA-specific manner.

28 ommonest HLA class I alleles in SE Asia) and HLA-C*01 were associated with an increased risk of death

29 HLA-DR15 and HLA-DR1 exhibit distinct peptide repertoires and binding

30 HLA-DR15(+) and HLA-DR1(+) healthy human donors display altered alpha313

31 genetic influence of the endogenous gene and HLA haplotype on the outcome of gene therapy.

32 In patients, KIR3DL1 and HLA-B subtype combinations that were predictive of weak

33 ffects of weak and noninhibiting KIR3DL1 and HLA-B subtype combinations were separate from and additi

34 ationship between gene transcript levels and HLA ligand presentation.

35 patibility complex-borne microsatellites and HLA-DPB1 alleles using DNA obtained from 318 anti-topois

36 genetic risk factors for MS (female sex and HLA risk haplotypes).

37 895-G with PD, and suggests that smoking and HLA-DRB1 are involved in common pathways, possibly relat

38 alpha3135-145 tetramer(+) Foxp3(-) Tconv and HLA-DR1-alpha3135-145 tetramer(+) Foxp3(+)CD25(hi)CD127(

39 Anti-HLA antibodies mean fluorescence intensity (MFI) values

40 Complement-activating anti-HLA donor-specific antibodies (DSAs) are associated with

41 knockdown, and they were not blocked by anti-HLA class I Abs, suggesting that KIR2DL3, in addition to

42 rades), immunostaining, and circulating anti-HLA donor-specific antibodies at the time of biopsy, tog

43 can occur in patients with preexisting anti-HLA donor-specific antibodies (DSA) or in patients who d

44 ial fibrosis and de novo donor specific anti-HLA antibodies (dnDSA) at 1 year.

45 lated to be activated by donor-specific anti-HLA antibodies triggering their CD16a Fc receptors.

46 are sensitised with human leucocyte antigen (HLA) antibodies.

47 s between classical human leukocyte antigen (HLA) alleles and common immune-mediated diseases (IMDs).

48 neoantigens through human leukocyte antigen (HLA) loss may facilitate immune evasion.

49 des ago, an unusual human leukocyte antigen (HLA) molecule was identified: HLA-G.

50 Additionally, the human leukocyte antigen (HLA) region was comprehensively studied by imputing clas

51 en positive for the human leukocyte antigen (HLA)-DQ2 and/or HLA-DQ8 from 5 European countries.

52 Human leukocyte antigen (HLA)-DQ2.5 (DQA1*05/DQB1*02) is a class-II major histoco

53 association between human leukocyte antigen (HLA)-DRB1 and the risk of PD.

54 ific alleles of the human leukocyte antigen (HLA)-DRB1 gene (HLA-DRB1) encode a "shared epitope" (SE)

55 man MHC-Ib molecule human leukocyte antigen (HLA)-E and specific for an epitope from UL40 (VMAPRTLIL)

56 Subcellular localization of antigen, HLA molecules, and tryptase was analyzed by using struct

57 Six subsets of phagocytic APC (HLA-DR(+)) were consistently observed.

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

59 fespan, the authors identify associations at HLA-DQA/DRB1 and LPA and find that genetic variants that

60 Maximal heterozygosity at HLA-I loci ("A," "B," and "C") improved overall survival

61 nt docking mode and molecular footprint atop HLA-E when compared with the TRBV14(+) TCR-HLA-E ternary

62 Because HLA-E plays an important role in antiviral immunity by r

63 ons, the probability of all 4 patients being HLA-B*53 carriers, and 2 of 3 African patients being hom

64 e complex structure of peptide-loaded beta2m-HLA-F bound to the inhibitory LIR1 revealed similarities

65 cohorts to examine the relationship between HLA haplotypes and AD risk in 309 individuals (191 AD, 1

66 ediated mechanisms targeting antigens beyond HLA may trigger and accelerate immune responses.

67 omplement binding from noncomplement binding HLA-specific antibodies have been introduced, but techni

68 o complexes with gHgL heterodimers and binds HLA class II to activate gB-mediated membrane fusion wit

69 ased negative impact when antibodies to both HLA and non-HLA antigens are present pretransplant.

70 D & AIMS: Celiac disease is characterized by HLA-DQ2/8-restricted responses of CD4+ T cells to cereal

71 individualized alloimmune risk determined by HLA-DR/DQ epitope mismatch.

72 expressed as a fraction of those induced by HLA nonidentical cells in parallel cultures.

73 44-KIR2DP1(F) with lysine 44 recognized C1(+)HLA-C, whereas T44-KIR2DP1(F) recognized C2(+)HLA-C.

74 LA-C, whereas T44-KIR2DP1(F) recognized C2(+)HLA-C.

75 Interestingly, these CD45(+)CD33(+)CD11b(+)HLA-DR(-) MDSCs exhibited increased CXCR2 expression com

76 x 106/l +/- 165 trauma, p < 0.0005) and CD14+HLA-DRlow/- monocytes (34.96 x 106/l +/- 4.48 control ve

77 ells; 95% CI = 1.01-2.05; P = .045) and CD38+HLA-DR+ CD8+ T cells (1.40 fold-change in integrated HIV

78 d immune activation (percentages of CD4+CD38+HLA-DR+ and CD8+CD38+HLA-DR+ T cells).

79 ercentages of CD4+CD28-, CD8+CD28-, CD4+CD38+HLA-DR+, and CD8+CD38+HLA-DR+ T cells, dehydroepiandrost

80 percentages of CD4+CD38+HLA-DR+ and CD8+CD38+HLA-DR+ T cells).

81 -, CD8+CD28-, CD4+CD38+HLA-DR+, and CD8+CD38+HLA-DR+ T cells, dehydroepiandrosterone sulfate, free te

82 tegrated HIV DNA per 1-unit increase in CD38+HLA-DR+ CD8+ T cells; 95% CI = 1.05-1.86; P = .02).

83 Characterizing HLA LOH with LOHHLA refines neoantigen prediction and ma

84 onsistent with the known impact of classical HLA alleles.

85 omoter region variation within the classical HLA class I loci.

86 ize circulating CD4(+) T cells in coinfected HLA-DR7(+) long-term nonprogressor HIV subjects with und

87 HLA-B*46 (one of the commonest HLA class I alleles in SE Asia) and HLA-C*01 were associ

88 Our data confirmed HLA class II as the strongest associated region (indepen

89 Denatured HLA was expressed as HC-10 binding to untreated SAB as a

90 tigen beads (SAB) is influenced by denatured HLA on SAB, antibody titre, and complement interference

91 ncoding the well-defined genotype 1a-derived HLA-A2-restricted HCV NS3-1073 or NS5-2594 epitope were

92 in cross-presentation of PR1, an NE-derived HLA-A2-restricted peptide that is an immunotherapy targe

93 pients treated with tacrolimus who developed HLA-DR/DQ dnDSA had a higher proportion of tacrolimus tr

94 subtype-specific determinant of differential HLA-A versus HLA-B downregulation activity.

95 Antibodies that are specific to organ donor HLA have been involved in the majority of cases of antib

96 with differential abilities to downmodulate HLA-C.

97 nconsensus variants at codon 9 downregulated HLA-B (though not HLA-A) significantly better than those

98 placed with the human leukocyte antigen DR4 (HLA-DR4).

99 ), MUC12, MUC4, MUC6, MUC2, SIRPA, HLA-DRB1, HLA-A and HLA-B molecules.

100 tly associated with class II genes (HLA-DRB1/HLA-DQA1) whereas TAK was mostly associated with class I

101 -restricted response targets Gag (DRYFKTLRA, HLA-B*14-DA9).

102 we identified 516 peptides that bind either HLA-A*02:01 or HLA-B*27:05.

103 Compared to empty HLA-F open conformers (OCs), HLA-F tetramers bound with

104 opulation of CD11b+ myeloid cells expressing HLA-DR, CD11c, and CX3CR1.

105 HIV are observed only in subjects expressing HLA-B*14:02, and not HLA-B*14:01.

106 inued to be significant after adjustment for HLA-DR/DQ eplet mismatch.

107 2 of 3 African patients being homozygous for HLA-B*53:01, is approximately 0.00002.

108 ng for HLA-A and HLA-B, and allele-level for HLA-DRB1.

109 onse over Gag, substantially more marked for HLA-B*14:02.

110 are preferentially matched with patients for HLA-A, -B, -C, and -DRB1.

111 All children and adults were positive for HLA-DQ2.5.

112 igen-level (lower resolution) HLA typing for HLA-A and HLA-B, and allele-level for HLA-DRB1.

113 = 135) or RIC (n = 137) followed by HCT from HLA-matched related or unrelated donors.

114 Simulations using 46 ICPs and 11 fully HLA-mismatched CPs were undertaken using the Australian

115 Furthermore, HLA-DR molecules encoded by shared-epitope (SE) alleles

116 with the major psoriasis-psoriasis risk gene HLA-C*06.

117 the human leukocyte antigen (HLA)-DRB1 gene (HLA-DRB1) encode a "shared epitope" (SE) associated with

118 AK was mostly associated with class I genes (HLA-B/MICA).

119 A was mostly associated with class II genes (HLA-DRB1/HLA-DQA1) whereas TAK was mostly associated wit

120 ab combined with alemtuzumab induction gives HLA-sensitized patients an opportunity for successful ki

121 We administered IdeS to 25 highly HLA-sensitized patients (11 patients in Uppsala or Stock

122 ctional analyses of the human H2-Ob homolog, HLA-DOB, revealed both loss- and gain-of-function allele

123 A homozygous HLA target does not trigger a twice higher XM positivity

124 Monocyte recruitment by human HLA antibodies was enhanced in the presence of intact hu

125 8(+) T-cell clones recognizing the identical HLA-B*2705-restricted HIV-1 epitope KK10 (KRWIILGLNK).

126 8(+) T-cell clones recognizing the identical HLA-B*2705-restricted HIV-1 Gag-derived peptide, KK10 (K

127 ocyte antigen (HLA) molecule was identified: HLA-G.

128 ta show that IFN-gamma induces HLA class II, HLA-DM, CD80, and CD40 expression on MCs, whereas MCs ta

129 histocompatibility complex class II (MHC-II; HLA-DR)-dependent manner.

130 ctive antibody ranging 70% to 80% to improve HLA matching in CP recipients.

131 nucleotide polymorphisms, as well as imputed HLA alleles and amino acids.

132 mic relapse, but capturing alloreactivity in HLA-matched HCT has been elusive.

133 LA-DR15-alpha3135-145 tetramer(+) T cells in HLA-DR15 transgenic mice exhibit a conventional T-cell p

134 pe recognition was not due to differences in HLA class II binding, memory phenotypes, or gene express

135 estimated risks of GVHD-related outcomes in HLA-phenotypically matched unrelated recipients were low

136 tation of IPF PBMC cultures also resulted in HLA-DR-dependent production of IgG with anti-vimentin sp

137 ymphoma (rs9269081, HLA-DPB1*03:01, Val86 in HLA-DRB1) and mixed cellularity Hodgkin lymphoma (rs1633

138 in lymphoma (rs1633096, rs13196329, Val86 in HLA-DRB1).

139 Our data show that IFN-gamma induces HLA class II, HLA-DM, CD80, and CD40 expression on MCs,

140 nded when a hepatitis C virus (HCV)-infected HLA-A2(-) individual received an HLA-A2(+) liver allogra

141 -resident T cells in TG of latently infected HLA-A*0201-transgenic mice and reduced recurrent ocular

142 nsduced HLA-A2(+) T cells efficiently killed HLA-A2(+)H3.3K27M(+) glioma cells in an antigen- and HLA

143 ication is determined by the strength of KIR/HLA-C interactions and is thus dependent on both host ge

144 totoxic NK potential on the basis of KIR3DL1/HLA-B subtype combinations in vitro and evaluated their

145 tric donor-recipient pairs with allele-level HLA matching who received a single unit umbilical cord b

146 e ubiquitous KIR3DL1 and its cognate ligand, HLA-B, would titrate NK reactivity against acute myeloge

147 nonuclear cells, mouse MAIT hybridoma lines, HLA-DR4-transgenic mice, MAIThighHLA-DR4+ bone marrow ch

148 cover two regions associated with longevity (HLA-DQA1/DRB1 and LPA).

149 surface expression of APC-associated markers HLA-DR and CD86.

150 st genetics and the extent of virus-mediated HLA-C downregulation.

151 from autoimmunity afforded by particular MHC/HLA alleles can operate via intestinal microbes, highlig

152 gh the involvement of tolerogenic molecules (HLA-G, TGF-beta, and IL-10) were tested on a mixed lymph

153 During CMV-CTL monitoring using mutated HLA/CMV tetramers selectively detecting high-avidity T c

154 -agent GVHD prophylaxis after myeloablative, HLA-matched related (MRD), or HLA-matched unrelated (MUD

155 Non-HLA antibodies (non-HLAabs) were screened in 29 transpla

156 Non-HLA antibody testing was included in the posttransplant

157 A non-HLA autoantibody combined with a preformed HLA DSA is as

158 e impact when antibodies to both HLA and non-HLA antigens are present pretransplant.

159 donor and recipient matching of HLA and non-HLA compatibility.

160 oconversion, INS gene (rs1004446_A), and non-HLA gene polymorphisms identified by the Type 1 Diabetes

161 Eight established non-HLA risk loci showed pleiotropic associations.

162 Biopsies with de novo non-HLA autoantibodies revealed a new sinusoidal C4d stainin

163 le candidate gene-association studies of non-HLA single-nucleotide polymorphisms (SNPs) and outcomes

164 in subjects expressing HLA-B*14:02, and not HLA-B*14:01.

165 s at codon 9 downregulated HLA-B (though not HLA-A) significantly better than those harboring the con

166 on (LT) recipients with preformed or de novo HLA donor-specific alloantibodies (DSA).

167 f the previously unappreciated role of H2-O (HLA-DO) in immunity to infections may suggest new approa

168 mpared to empty HLA-F open conformers (OCs), HLA-F tetramers bound with human-derived peptides differ

169 Therefore, the absence of HLA-DR7 or HLA-DRB4 could raise tumor suspicion in anti-

170 , NK cells were able to sense alterations of HLA-C expression demonstrated by increased antiviral act

171 e that causes a misleading low assessment of HLA-specific antibody levels.

172 independent of the well-known association of HLA antigen MMs with graft survival.

173 These results suggest that the capability of HLA-C-licensed NK cells to control HIV-1 replication is

174 s directed at cancer neoantigens, a class of HLA-bound peptides that arise from tumour-specific mutat

175 s before dnDSA development in the context of HLA-DR/DQ eplet mismatch.

176 degranulation increases surface delivery of HLA class II/peptide, further enhancing stimulation of T

177 Development of HLA-E-targeted therapies will require a physiologically

178 CD8(+) T cells, epigenetic downregulation of HLA-E by high-risk HPV E7 may contribute to virus-induce

179 asis for the dominantly protective effect of HLA in autoimmune disease, whereby HLA polymorphism shap

180 unrelated HCT is predominantly an effect of HLA-mismatching.

181 ion 71, within the peptide-binding groove of HLA-DRB1 (P = 2 x 10(-4) ).

182 The impact of HLA mismatches on graft survival was analyzed and surviv

183 Inclusion of HLA analyses did not increase accuracy.

184 In contrast to re-induction of HLA class-I by interferons, HDAC inhibitors did not inte

185 with HLA-DQ2, suggesting the involvement of HLA-DQ2-restricted gluten-specific CD4(+) T cells.

186 s have seen an explosion in our knowledge of HLA-G biology.

187 host's immuno-surveillance, e.g. by loss of HLA class-I expression.

188 precision of donor and recipient matching of HLA and non-HLA compatibility.

189 Neutralization of HLA-G, TGF-beta, and IL-10 partially restored T cell all

190 lymorphism of Papa-B, the bonobo ortholog of HLA-B, for six wild bonobo populations.

191 positions in the peptide-binding pockets of HLA-DRB1 molecule account for a significant incremental

192 yclonal or DeltaCAR Tregs in the presence of HLA-A2, without eliciting cytotoxic activity.

193 Given the approximate prevalence of HLA-B*53 carriage in African (20%) and Hispanic (6%) pop

194 tigen hierarchy, and had similar profiles of HLA restriction.

195 , it was concluded that the survival rate of HLA poorly matched living donor transplants is not infer

196 hes (MMs) at the antigen recognition site of HLA molecules represent independent and incremental risk

197 ) T cell clone established by stimulation of HLA-A2(+) CD8(+) T cells with synthetic peptide encompas

198 tivating NK receptors or upregulated that of HLA class I, B7-H3, PD-L1, and PD-L2, molecules that mig

199 donor transplants is not inferior to that of HLA well-matched deceased donor transplants.

200 Upregulation of HLA-DR on neutrophils required the presence of the antig

201 o the presence of conformational variants of HLA-I on SAB, assessment of which would increase the con

202 We collected data on HLA-DR, DQ genotypes of 31,766 infants, born from 1993 t

203 atients who were homozygous for at least one HLA locus.

204 ary AAV cassettes containing codon optimized HLA-G1 (transmembrane) or HLA-G5 (soluble) isoforms were

205 516 peptides that bind either HLA-A*02:01 or HLA-B*27:05.

206 the human leukocyte antigen (HLA)-DQ2 and/or HLA-DQ8 from 5 European countries.

207 n of multiple viruses included cord blood or HLA-mismatched HCT, myeloablative conditioning, and acut

208 Therefore, the absence of HLA-DR7 or HLA-DRB4 could raise tumor suspicion in anti-LGI1 patien

209 myeloablative, HLA-matched related (MRD), or HLA-matched unrelated (MUD) donor T-cell-replete bone ma

210 ng codon optimized HLA-G1 (transmembrane) or HLA-G5 (soluble) isoforms were validated in vitro.

211 the new distributed representation with our HLA-CNN architecture achieves state-of-the-art results i

212 bound peptide, leaving open whether peptide-HLA-F-specific T and NK receptors exist.

213 somal regulation of tumor-associated peptide/HLA antigen complexes, and yield possible therapeutic so

214 monomorphic nature in the human population, HLA-E is an attractive target for novel vaccine and immu

215 CD14(pos)HLA-DR(low/neg) monocytic (M)-MDSCs were expanded in int

216 ependent cellular cytotoxicity against PRAME+HLA-A2+ leukemia cells and was therapeutically effective

217 To achieve this, we predicted HLA class I- and class II-restricted peptides from rDEN2

218 n-HLA autoantibody combined with a preformed HLA DSA is associated with an increased mortality risk.

219 in vitro Among persons expressing protective HLA class I alleles, carriage of Nef codon 9 variants wa

220 ral load (HR = 2.9; P = 0.004) or protective HLA alleles (HR = 0.61; P = 0.36).

221 kedly increased disease risk, the protective HLA-DR1 allele is dominantly protective in trans with HL

222 lly relevant animal model that recapitulates HLA-E-restricted T cell biology.

223 LIR1, however, recognized HLA-F away from bound peptide, leaving open whether pept

224 Indeed, a reduced HLA class-I expression was observed in MCC tumor tissues

225 molecule, but not within the closely related HLA-B*35:01 molecule.

226 Purpose T-cell-replete HLA-haploidentical donor hematopoietic transplantation u

227 s relies on antigen-level (lower resolution) HLA typing for HLA-A and HLA-B, and allele-level for HLA

228 Thus, HDAC inhibition restored HLA class-I surface expression in vitro and in a mouse x

229 ll therapy using an MHC class II-restricted, HLA-DPB1*0401-restricted TCR that recognized the cancer

230 antibody positivity, sex, selected high-risk HLA-DR-DQ genotypes, relationship to a family member wit

231 dular sclerosis Hodgkin lymphoma (rs9269081, HLA-DPB1*03:01, Val86 in HLA-DRB1) and mixed cellularity

232 ale immunoisolation of the antigen serotypes HLA-A*02:01 and HLA-B*27:05 expressed on the Epstein-Bar

233 The most significant HLA association was the previously reported amino acid v

234 .a. CA-125), MUC12, MUC4, MUC6, MUC2, SIRPA, HLA-DRB1, HLA-A and HLA-B molecules.

235 Specific HLA-A alleles varied in the usage of the proximal versus

236 ne together with reduction of donor-specific HLA antibodies (DSA) below 500 mean fluorescence intensi

237 We demonstrate that Env-specific HLA-B*14-restricted activity is substantially more effic

238 with consistently low expression of specific HLA class I antigens.

239 The strong HLA association seems not applicable in these patients.

240 A subdominant HLA-B*14-restricted response targets Gag (DRYFKTLRA, HLA

241 tially more efficacious than the subdominant HLA-B*14-restricted Gag response.

242 Only 1 cellular target HLA antigen for the serum was expressed in 238 cases, 20

243 p HLA-E when compared with the TRBV14(+) TCR-HLA-E ternary complex.

244 trongly associated with viremic control than HLA-B*14:01.

245 potent at inhibiting viral replication than HLA-B*14-DA9.

246 t humoral and cellular immune responses than HLA-DR4 mice.

247 We hypothesized that HLA class II de novo donor-specific antibody (dnDSA) dev

248 These structures revealed that HLA-C*06:02 possesses a deep peptide-binding groove comp

249 e-saporin-conjugated tetramers, we show that HLA-B*14-EL9 is substantially more potent at inhibiting

250 Finally, we show that HLA-B*14:02 is significantly more strongly associated wi

251 evels can receive transplantation across the HLA-barrier, with the use of an intensified posttranspla

252 ulin B-chain (InsB) epitope presented by the HLA-DQ8 molecule associated with high T1D risk.

253 n with HLA class II alleles encoding for the HLA DQ2.5 molecule.

254 clude that although genetic variation in the HLA region is important to the aetiology of many disorde

255 notyping of the rs660895 polymorphism in the HLA-DRB1 region was based on saliva or blood DNA samples

256 netic differences between GCA and TAK in the HLA.

257 THODS AND Building on prior work linking the HLA to AD, we used a robust imputation method on two sep

258 Silencing of the HLA class-I APM is due to histone deacetylation as inhib

259 are the complex genetic organization of the HLA region, differences in sequencing and allelic imputa

260 tistical significance and effect size of the HLA signals were considerably reduced in the cross-disea

261 rmed expression of two distinct forms of the HLA-A 3'UTR based on use of either the proximal or the d

262 bind within the antigen binding cleft of the HLA-B*53:01 molecule, but not within the closely related

263 etermined the X-ray crystal structure of the HLA-DQ2.5.

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

265 Outside the HLA region, only one polymorphism located nearby the IL1

266 the principles of population genetics to the HLA genes has resulted in the development of a numeric m

267 switching, and ten new associations with the HLA region.

268 ctures of a TRBV9(+) TCR in complex with the HLA-E molecule presenting the two peptides.

269 Additionally, independent loci within the HLA region are observed for nodular sclerosis Hodgkin ly

270 lucidated the peptide specificities of these HLA molecules using a comprehensive analysis of naturall

271 Functional analysis showed that this HLA-C*06:02-presented peptide can furthermore activate p

272 examined the extent to which C1q-binding to HLA-class I single-antigen beads (SAB) is influenced by

273 s well as beta2m, thus precluding binding to HLA-F OCs.

274 trongest genetic association was intronic to HLA-DQA1 (rs9272622; P = 1.86 x 10-7).

275 In contrast to HLAs, which are constitutively expressed on the cell sur

276 that KIR2DL3, in addition to the traditional HLA-C ligands, can bind to the same beta2-microglobulin-

277 TCR-transduced HLA-A2(+) T cells efficiently killed HLA-A2(+)H3.3K27M(+

278 l inoculation of medroxyprogesterone-treated HLA-DR4 transgenic mice with 5 x 10(5)C. trachomatis D i

279 lcipotriol plus 5-FU treatment induced TSLP, HLA class II, and natural killer cell group 2D (NKG2D) l

280 ion of a transplant candidate's unacceptable HLA antigens.

281 -145-specific T-cell antigen receptor usage, HLA-DR15-alpha3135-145 tetramer(+) Foxp3(-) Tconv and HL

282 flation occurs during HIV infection, we used HLA-DR7 (DRB1*07:01) tetramers loaded with the glycoprot

283 Using HLA-B*14/peptide-saporin-conjugated tetramers, we show t

284 ESO) and the human leukocyte antigen variant HLA-A*0201 (A2) as a model and predicted in silico the 4

285 fic determinant of differential HLA-A versus HLA-B downregulation activity.

286 61 patients were enrolled, 42 were HLA matched and 19 were haploidentical.

287 Clinical parameters analyzed were: HLA antibodies at transplant, de novo donor-specific ant

288 between these two diseases was observed when HLA variants were tested.

289 effect of HLA in autoimmune disease, whereby HLA polymorphism shapes the relative abundance of self-e

290 While HLA-DR15 confers a markedly increased disease risk, the

291 ial cell crossmatch (ECXM) in patients whose HLA antibody level was insufficient to cause a positive

292 ulocapillary miRNA signature associated with HLA class I-DSA could improve our understanding of ABMR

293 Like CD, RCDII is strongly associated with HLA-DQ2, suggesting the involvement of HLA-DQ2-restricte

294 t analyses showed a primary association with HLA class II alleles encoding for the HLA DQ2.5 molecule

295 idal C4d staining pattern when compared with HLA DSA (71% vs 3%; P < 0.001).

296 sed tetramer(+) CD4(+) T cells compared with HLA-matched control subjects without diabetes.

297 ocking strategy that relies on contacts with HLA-F as well as beta2m, thus precluding binding to HLA-

298 L-2R levels were also found in patients with HLA-B27-associated (4460 [2465] pg/mL) and varicella-zos

299 These preferences are shared with HLA-B*27 and Mamu-B*008, molecules shown to be involved

300 llele is dominantly protective in trans with HLA-DR15 (ref.