ライフサイエンスコーパス: HLA

1 HLA alleles may be factors that influence phenotypes alo

2 HLA antibodies pose a significant barrier to transplanta

3 HLA class I associations are often interpreted in the li

4 HLA class II alleles encode MHC proteins on antigen-pres

5 HLA molecules of the MHC class II (MHCII) bind and prese

6 HLA typing can be fast and inexpensive.

7 HLA upregulation in response to aberrant viral RNAs coul

8 HLA-DQA1 and -DQB1 genes have significant and potentiall

9 HLA-DRB1*10:01 predisposed to immediate hypersensitivity

10 HLA-specific memory B cells may contribute to the serum

11 Study 1 randomly assigned (1:1) HLA-B*5701-negative adults without hepatitis B virus co-

12 tivation proteins, including ICAM-1, VCAM-1, HLA class I and II, and interferon gamma receptor.

13 conserved epitopes and were restricted to 13 HLA class I genotypes, hence providing high coverage amo

14 tide-MHC class I binding affinity across 145 HLA-A, -B, and -C genotypes for all SARS-CoV-2 peptides.

15 c for the cancer testis Ag NY-ESO-1(157-165)-HLA-A2.

16 offspring or a nonoffspring, with exactly 3 HLA matches, as would be expected between an offspring a

17 We evaluated the relationship between 44 HLA class I and 28 class II alleles and percentages of a

18 to profile >185,000 peptides eluted from 95 HLA-A, -B, -C and -G mono-allelic cell lines.

19 GWAS identified a HLA region associated with NMO, led by rs9272219 (OR = 2

20 C) class I genes (human leukocyte antigen A [HLA-A], -B, and -C genes) may affect susceptibility to a

21 ly matched or one-locus mismatched at HLA-A, HLA-B, HLA-C, or DRB1 loci) graft following myeloablativ

22 Fifty-four ABO/HLA compatible pairs participated in KPD for the followi

23 donor kidney transplantation (ILDKT) across HLA/ABO barriers, but added immunomodulation might put p

24 n 6) and levels of T-cell immune activation (HLA-DR+CD38+).

25 In this phase 1 and 2 trial, we administered HLA-mismatched anti-CD19 CAR-NK cells derived from cord

26 role of the leader dimorphism in GVHD after HLA-B-mismatched unrelated HCT.

27 Donor-specific antibodies (DSA) against HLA and non-HLA antigens in the glomeruli and the tubulo

28 on one of the most prevalent HLA-B alleles, HLA-B*52:01, present in 22.5% of infected individuals.

29 Recipients of an HLA-DR1 donor also have an impaired cardiovascular outco

30 Patients age 13 years or older with an HLA-matched sibling donor or age 12 years or younger wit

31 ing donor or age 12 years or younger with an HLA-matched unrelated donor were at intermediate risk (3

32 differential association of HLA-B*57:01 and HLA-B*57:03 with the control of HIV, recognition of thes

33 this study, we have used rHLA-DRB1*01:01 and HLA-DRB1*03:01 molecules to interrogate high-density pep

34 In the EA population, the HLA-DPB1*13:01 and HLA-DRB1*07:01 alleles were more strongly associated wit

35 alleles expressed in humans, HLA-E*01:01 and HLA-E*01:03, can lead to the activation of unconventiona

36 Lacandon population include HLA-A*24:14 and HLA-B*40:08.

37 the antigen-binding clefts of HLA-DQ2.5 and HLA-DQ2.2 are very similar, differences in the nature of

38 udies with C57BL/6; RAG1(-/-) (C57BL/6); and HLA-DQ8, huCD4 transgenic Ab0 NOD mice.

39 Global immune activation and HLA alleles are each associated with the pathogenesis of

40 In addition, CD4(+) T cells and HLA-DQ8 have a crucial role in the licensing of cytotoxi

41 cells and CTLs, and between tumor cells and HLA-DR(+) macrophages, but not HLA-DR(-) macrophages.

42 A at 1 year was 0.84 and 0.82 for HLA-DR and HLA-DQ eplet mismatches, respectively.

43 sulted in reduced expression of HLA-DRB1 and HLA-DQA1 genes.

44 ppressive human leukocyte antigens HLA-G and HLA-F are expressed on trophoblast and malignant cells.

45 prognostic and predictive value of HLA-G and HLA-F protein isoform expression patterns in patients wi

46 no pathophysiologically relevant gluten- and HLA-dependent preclinical model exists.

47 ested the ability of the NMDP HaploStats and HLA Matchmaker programs to impute/reproduce the measured

48 pression and secretion of IFNgamma, IDO, and HLA-G.

49 MP) vs. asymptomatic (ASYMP) individuals and HLA-A*0201 transgenic rabbits.

50 ls, with inducible costimulator molecule and HLA-DR defining midterm and long-term T-cell activation,

51 associated with HLA class I region only and HLA class II region only, implying the importance of cyt

52 nti-human leukocyte antigen antibodies (Anti-HLA Ab) for donor-recipient matching and patient risk st

53 linical relevance of complement-binding anti-HLA antibodies remains unclear.

54 d alloimmune response as represented by anti-HLA sensitization.

55 sted for total IgG and IgG1-4 by ELISA, anti-HLA-total IgG, IgG3 and IgG4, and donor-specific antibod

56 cacy in eliminating BM PCs and reducing anti-HLA Abs in chronically HLA-sensitized patients; however,

57 The impact of donor-specific anti-HLA antibodies (DSA) on antibody-mediated rejection (AMR

58 nonuclear cells (PBMCs) pretreated with anti-HLA antibody positive (HS) or negative (NC) sera to meas

59 une responses to nonhuman leukocyte antigen (HLA) after cardiac transplantation to identify antibodie

60 NPs) and 38 imputed Human Leukocyte Antigen (HLA) alleles were analyzed through a genome-wide associa

61 regions such as the human leukocyte antigen (HLA) and killer cell immunoglobulin-like receptor (KIR)

62 sely identify tumor human leukocyte antigen (HLA) bound peptides capable of mediating T cell-based tu

63 nship of protective human leukocyte antigen (HLA) class I alleles and HIV progression is well defined

64 stance is linked to human leukocyte antigen (HLA) class I/II variants and their individual capacity t

65 s III region of the human leukocyte antigen (HLA) complex in the South Asian dataset that clearly rep

66 from alleles of the human leukocyte antigen (HLA) genes at that locus(3-6).

67 The human leukocyte antigen (HLA) haplotype reference panel used for calculation of t

68 ranscripts encoding human leukocyte antigen (HLA) receptors as well as B cell and T cell receptors (B

69 ptides presented by human leukocyte antigen (HLA).

70 e immunosuppressive human leukocyte antigens HLA-G and HLA-F are expressed on trophoblast and maligna

71 mmunity.IMPORTANCE Human leukocyte antigens (HLAs) are cell surface proteins that regulate innate and

72 These results suggest that any HLA or C4 variants associated with depression either are

73 Patients who are HLA-A*01:01pos could benefit from such products, since n

74 hy occurs exclusively in individuals who are HLA-A29 positive.

75 of pharmacogenetic screening tests, such as HLA-B*57:01 in abacavir therapy, which has successfully

76 nt HLA class I and II antibodies, as well as HLA-DR1 donor/recipient genotype and the primary (major

77 rations might account for the association at HLA-DRB1, independent of the previously reported HLA-DPB

78 mplete knowledge of the genetic diversity at HLA and BCR/TCR loci.

79 gests a potential effect on T-lymphocytes at HLA-B(*)55:01.

80 or (fully matched or one-locus mismatched at HLA-A, HLA-B, HLA-C, or DRB1 loci) graft following myelo

81 hed or one-locus mismatched at HLA-A, HLA-B, HLA-C, or DRB1 loci) graft following myeloablative or no

82 Both short-read RNA-seq-based HLA typing and BCR/TCR repertoire sequencing (AIRR-seq)

83 e converted high-resolution, sequence-based, HLA typing of 310 subjects from an ethnically heterogene

84 rt did not differ overall (p = 0.14) between HLA-A29 positive and negative subjects, although some di

85 peptide analogue with high affinity for both HLA-B*08 and the ERAP1 active site could not promote the

86 rbation of the natural peptides displayed by HLA-B*57:01.

87 es within proinsulin, which are presented by HLA class II molecules associated with T1D risk.

88 s of shared and tumor-specific non-canonical HLA peptides, including an immunogenic peptide derived f

89 ated with infliximab monotherapy who carried HLA-DQA1*05; conversely the lowest rates of immunogenici

90 imumab combination therapy who did not carry HLA-DQA1*05.

91 model, we observed that individuals carrying HLA class I genotypes characterized by greater tapasin i

92 Accumulation of CD14(+)HLA-DR(low) monocytic MDSCs has been described in newly

93 D163(+)CSF1R(+) at higher levels than CD68(+)HLA-DR(+) macrophages, consistent with an M2 phenotype.

94 In pathogen-infected cells, HLA class I expression is perturbed.

95 ression of HLA-DR in tumor epithelial cells; HLA-DR expression was also significantly higher in the t

96 PCs and reducing anti-HLA Abs in chronically HLA-sensitized patients; however, Ab rebound was observe

97 oth buried within the peptide-binding cleft, HLA-B*57:01 more potently inhibited NK cell activation.

98 izing any EBV-derived peptide in this common HLA allele have been found thus far.

99 nce of antiretroviral treatment, we compared HLA-B*57:01-restricted HIV-specific CD8 T-cell responses

100 When considering HLA-mismatched transplantation for Hodgkin or non-Hodgki

101 at CLEC16A participates in the BCR-dependent HLA-II pathway in human B cells and that this regulation

102 current donor-specific memory B cell-derived HLA antibodies (DSA-M) in renal allograft recipients wit

103 ment with EBV-CTLs restricted by a different HLA allele (switch therapy) can also induce remissions i

104 likely occurs in conjunction with different HLA-DP binding groove conformations.

105 We discovered HLA risk factors and four non-HLA susceptibility loci in

106 flow crossmatch (DSA-FXM) that distinguishes HLA class I or II donor-specific antibody bound to HLA a

107 Human leukocyte antigen-DM (HLA-DM) is an integral component of the major histocompa

108 preformed HLA class II antibodies and donor HLA in kidney transplant recipients (KTRs) remain unesta

109 ed patient is attributed to mismatched donor HLA.

110 tional FXM results are not directed to donor HLA 60.25% of the time and negative traditional FXM resu

111 immunopeptidome analysis delineate how drug HLA-B*57:01 binding and peptide display by antigen prese

112 mouse homolog of human leukocyte antigen-E (HLA-E), inhibits antibody-mediated immune rejection of h

113 Here, we present Easy-HLA, a web-based software suite designed to facilitate a

114 ly associated with the abundance of effector HLA-DR(+)CD8(+) T cells.

115 y cross-recognized variant epitopes encoding HLA-I-associated adaptations, further supporting our con

116 To enable prediction of endogenous HLA class I-associated peptides across a large fraction

117 These models predicted endogenous HLA class I-associated ligands with 1.5-fold improvement

118 Likewise, enhanced HLA-I APM expression was detected in RIG-Ihi (DDX58hi) m

119 that specifically binds to the NPM1c epitope-HLA-A2 complex but not to HLA-A2 or to HLA-A2 loaded wit

120 Despite this, many individuals expressing HLA risk alleles do not develop hypersensitivity when ex

121 cell research has largely focused on the few HLA alleles prevalent in a subset of ethnic groups.

122 For HLA-Upgrade, we reached a prediction accuracy of 92% fro

123 urve for DSA at 1 year was 0.84 and 0.82 for HLA-DR and HLA-DQ eplet mismatches, respectively.

124 ptide of preproinsulin is a major source for HLA class I autoantigen epitopes implicated in CD8 T cel

125 facilitate analysis and gain knowledge from HLA typing, regardless of nomenclature or typing method.

126 Splenocytes from HLA-DQ8 transgenic mice given TIMP-GLIA nanoparticles, b

127 ajor histocompatibility complex (MHC) I gene HLA-B in the occurrence of penicillin allergy.

128 Therefore, the capacity of given HLA class I/II variants to bind pathogen-derived peptide

129 T cells were activated, reflected as higher HLA-DR and CD38 expression.

130 l responses which are restricted by the host HLA class I allotype.

131 between the two alleles expressed in humans, HLA-E*01:01 and HLA-E*01:03, can lead to the activation

132 Associations with class I HLA variants are novel as they implicate adaptive immuni

133 cells cross-reacted with allogeneic class-I HLA molecules.

134 pression of the tumor-intrinsic HLA class I (HLA-I) antigen processing and presentation machinery (AP

135 ch significantly reduced both class I and II HLA antibodies and increased the likelihood of identifyi

136 this spectrum as we found new class I and II HLA associations for PFAPA distinct from Behcet's diseas

137 cted to bind a broad range of class I and II HLA molecules were selected for in vitro screening again

138 let autoantibodies, irrespective of class II HLA DR-DQ genotype.

139 model endogenously expressing MHC class II (HLA-DR), this study shows that HCMV decreases the expres

140 In HLA-B*57:03, the charged POmega-2 residues protruded out

141 to 4 acute GVHD could be reduced to <70% in HLA class I or II mismatched HCT.

142 consistent with higher rates of apoptosis in HLA-E(high) T cells in the presence of NKG2C(pos) NK cel

143 The decrease in HLA-DR expression was independent of the expression of p

144 usion protein was found to be immunogenic in HLA-B*40:01+ donors.

145 ular levels of caspase 3/7 were increased in HLA-E(high) Jurkat cells compared with HLA-E(low) Jurkat

146 H3.3K27M mutation as a shared neoantigen in HLA-A*02.01+, H3.3K27M+ DMGs.

147 CD8 T-cell population were apparent only in HLA-B*57-negative patients.

148 (and viral) genetics (including variation in HLA genes) in the immune response to coronaviruses, as w

149 s present in the Lacandon population include HLA-A*24:14 and HLA-B*40:08.

150 ed gene signature in monocytes and increased HLA-DR, CD80, CD86, and PD-L1 expression.

151 AV minireplicon were sufficient for inducing HLA upregulation.

152 e HSV-1 epitope-specificities, from infected HLA-A*0201 positive symptomatic (SYMP) vs. asymptomatic

153 rentiation of the trophoblast organoids into HLA-G+ EVT cells which rapidly migrate and invade throug

154 riptional suppression of the tumor-intrinsic HLA class I (HLA-I) antigen processing and presentation

155 rder with unknown etiopathogenesis involving HLA-related immune-mediated responses and environmental

156 8RAP axis and antigen presentation involving HLA-DRB1, which might help to identify potential therape

157 We also developed a KIR3DL1/HLA interaction strength metric and found that weak KIR3

158 strength metric and found that weak KIR3DL1/HLA interactions were associated with rigidity (p(c) = 0

159 nd expressed high levels of the NKG2C ligand HLA-E.

160 Interestingly, evidence links HLA alleles associated with high risk for autoimmune dis

161 Antigen-presenting cells had low HLA-DR and CD86 expression, potentially indicative of im

162 ; a T helper 2 signature; recruitment of low HLA-DR expressing monocytes and regulatory T-cells; and

163 lity of next-generation sequencing have made HLA typing from standard short-read data practical.

164 early-stage MDSCs and >40% monocytic MDSCs (HLA-DR(-)CD14(+)MDSCs).

165 nsisted of >35% ARG1-expressing naive MDSCs (HLA-DR(-)CD33(-)CD11b(-)CD14(-)CD15(-)MDSCs), >15% early

166 populations, we used genome-wide microarray, HLA high-resolution typing and AQP4 gene sequencing data

167 negative traditional FXM results are missing HLA donor-specific antibody 36.2% of the time based on t

168 multivariate Cox proportional hazard model, HLA class II antibodies before transplantation were asso

169 ilized version of the human class I molecule HLA-A*02:01 that is stable in the absence of peptide and

170 n via the nonclassical MHC class Ib molecule HLA-E, with nearly complete identity between the two all

171 lling center effects identified four or more HLA mismatches (hazard ratio [HR], 2.06; P <= 0.01) as a

172 ic CD8(+) T cell repertoires across multiple HLA-B7(+) individuals, indicating a shared Ag-driven bia

173 lated from healthy donors killed CBFB-MYH11+ HLA-B*40:01+ AML cell lines and primary human AML sample

174 No HLA alleles or C4 haplotypes were associated with depres

175 Antibodies to 4/18 non-HLA antigens synergize with HLA donor-specific antibodie

176 Protein microarray identified 366 non-HLA antibodies (>1.5 fold, P < .5) from a discovery coho

177 ted for reactivity against a panel of 44 non-HLA autoantigens.

178 pecific antibodies (DSA) against HLA and non-HLA antigens in the glomeruli and the tubulointerstitium

179 k to identify other predisposing HLA and non-HLA loci is required.

180 We discovered HLA risk factors and four non-HLA susceptibility loci in VPS8, SVEP1, CFL2, and chr13q

181 Recently, the relevance of non-HLA antibodies has become more prominent as AMR can be d

182 that multiplex bead array assessment of non-HLA antibodies identifies cardiac transplant recipients

183 mor cells and HLA-DR(+) macrophages, but not HLA-DR(-) macrophages.

184 sting tools and correctly identified >75% of HLA-bound peptides that were observed experimentally in

185 rformed tandem mass spectrometry analysis of HLA class I-bound peptides from 35 PDAC patient tumors.

186 This finding was replicated by analysis of HLA serotypes in 338 individuals with membranoproliferat

187 Given the differential association of HLA-B*57:01 and HLA-B*57:03 with the control of HIV, rec

188 ailable assays to evaluate the attributes of HLA antibodies and their utility both as clinical diagno

189 Characterization of HLA-G+ EVT from term pregnancy compared to first trimest

190 ar surfaces of the antigen-binding clefts of HLA-DQ2.5 and HLA-DQ2.2 are very similar, differences in

191 1.5 fold, P < .5) from a discovery cohort of HLA antibody-negative, endothelial cell crossmatch-posit

192 Detection of HLA antibodies (Ab) was performed by Luminex assay.

193 mory; and (3) progress in the development of HLA molecular mismatch computational scores as a potenti

194 Finally, we reported global distributions of HLA types with potential epidemiological ramifications i

195 pecificities is hindered by the diversity of HLA alleles (>20,000) and the complexity of many pathoge

196 e of the composition or genetic diversity of HLA and BCR/TCR loci.

197 The protein expression of HLA isoforms did not significantly differ between breast

198 shows that HCMV decreases the expression of HLA-DR in infected cells by reducing the transcription o

199 subset of TNBCs have elevated expression of HLA-DR in tumor epithelial cells; HLA-DR expression was

200 f DR/DQ-SE resulted in reduced expression of HLA-DRB1 and HLA-DQA1 genes.

201 g binds within the peptide binding groove of HLA-B*57:01 altering peptides displayed on the cell surf

202 Furthermore, immunization of HLA-DR transgenic mice with a mixture of the two immunod

203 Immunization of HLA-DR transgenic mice with a mixture of these two immun

204 rall SSc risk, emphasizing the importance of HLA in defining autoantibody subtypes.

205 Imputation of HLA types mapped this signal to a haplotype incorporatin

206 To gain insight into the influence of HLA-B*57:01 on the deterioration of CD8 T-cell responses

207 gression is well defined, the interaction of HLA-mediated protection and CD8 T-cell exhaustion is les

208 Expression levels of HLA-F and -G were correlated with the pathological compl

209 fic CD8 T cells promoted a selective loss of HLA-E(high) CD8 T cells.

210 However, the mechanisms of HLA-B*52:01-mediated immune control have not been well s

211 Higher number of HLA mismatches between the VA donor and the recipient, a

212 oss 27 cancer types suggest that patterns of HLA Class I and Class II associations may provide etiolo

213 surface, increasing surface presentation of HLA proteins known to inhibit the activation of an immun

214 significantly increased the presentation of HLA-B, -C, and -E on lung epithelial cells.

215 y epitope datasets covering a broad range of HLA alleles.

216 ltivariate regression models for the role of HLA mismatching on outcome.

217 ng the binding of peptides to a selection of HLA-I allomorphs.

218 stal structures of the peptide-free state of HLA-A*02:01, together with structures that have dipeptid

219 ng tolerance in a heterogeneous (in terms of HLA status) population of T1D patients, to the immunocom

220 ected cells by reducing the transcription of HLA-DR transcripts early during infection independently

221 luate the prognostic and predictive value of HLA-G and HLA-F protein isoform expression patterns in p

222 sed manner via single-cell RNA sequencing on HLA-DR(+) cells sorted from human lungs.

223 Early findings implicate not only HLA, particularly the HLA-DQA1 to HLA-DQB1 region, but a

224 l responses to responses restricted by other HLA class I alleles longitudinally after control of peak

225 Pairing HLA typing with COVID-19 testing where feasible could im

226 he use of banked VSTs derived from partially HLA-matched donors has shown efficacy in multicenter set

227 y the vaccine were predicted to bind patient HLA haplotypes.

228 structures and, using a single-chain peptide-HLA phage library, we generated peptide specificity prof

229 We determined TCR-peptide-HLA crystal structures and, using a single-chain peptide

230 newly developed peptide-exchangeable peptide/HLA multimers and artificial antigen-presenting cells fo

231 emonstrated a relationship between predicted HLA-B*57:01 binding orientations and the ability to indu

232 Further work to identify other predisposing HLA and non-HLA loci is required.

233 negative cardiovascular effects of preformed HLA class II antibodies and donor HLA in kidney transpla

234 e-adjusted association between pretransplant HLA class I and II antibodies, as well as HLA-DR1 donor/

235 cohort in Delhi on one of the most prevalent HLA-B alleles, HLA-B*52:01, present in 22.5% of infected

236 Reduced HLA class I expression is detected by KIR and CD94:NKG2A

237 and graft rejection rates in living-related HLA-identical (LR HLAid) renal transplantation.

238 DRB1, independent of the previously reported HLA-DPB1 variants.

239 mpute/reproduce the measured high-resolution HLA type, using the more common "winner-takes-all" appro

240 llow up on the earlier analysis on high-risk HLA-DQ2.5 and DQ8.1, the current analysis uncovers seven

241 -infected patients in Japan sharing the same HLA genotypes.

242 pressed self-antigens in the context of self-HLA can be found in the T-cell repertoire of healthy don

243 These results show that self-HLA-restricted T cells specific for self-antigens such a

244 uman leukocyte antigen with the A2 serotype (HLA-A2) that has been observed in about 35% of patients

245 -M might be a novel tool to supplement serum HLA antibody analysis for pretransplant risk stratificat

246 c memory B cells may contribute to the serum HLA antibody pool upon antigen reexposure.

247 The HLA typing of the patient showed HLA-DQ8, which was previously described as SHP-sensitive

248 d with a higher binding score for a specific HLA allotype does not necessarily imply it will be immun

249 recipients with pretransplant donor-specific HLA antibodies (DSA) and its association with occurrence

250 Renal function and donor-specific HLA-antibodies remained similar in both groups.

251 es suggest that non-canonical tumor-specific HLA peptides derived from annotated non-coding regions c

252 gs indicate that aberrant IAV RNAs stimulate HLA presentation, which may aid viral evasion of innate

253 cells resulted in an upregulation of surface HLA-DR and CD74 (invariant chain), whereas CLIP was slig

254 rect T cells to kill tumor cells with target HLA/peptide on their surfaces in vitro.

255 However, we found that HLA-B*46:01 had the fewest predicted binding peptides fo

256 We hypothesize that HLA-A29 may predispose chorioretinitis via an altered gu

257 The HLA and AIRR analysis approaches we introduce here are u

258 The HLA system plays a pivotal role in both clinical applica

259 The HLA typing of the patient showed HLA-DQ8, which was prev

260 The HLA-B*57:01-restricted, HIV epitope-specific CD8 T-cell

261 The HLA-DQA1*05 allele, carried by approximately 40% of Euro

262 The HLA-DR(-) subset coexpressed CD163(+)CSF1R(+) at higher

263 The HLA-DR15 haplotype is the strongest genetic risk factor

264 at peptide position 1 predicted to alter the HLA Trp-167 side-chain conformation abrogated TCR bindin

265 /A3 peptidome of beta-cells, we analyzed the HLA-A3-restricted peptides targeted by circulating CD8(+

266 ociations with KSHV antibody response in the HLA-B/C region (p = 6.64 x 10(-09)).

267 Building on our previous description of the HLA-A2/A3 peptidome of beta-cells, we analyzed the HLA-A

268 of the peptide-binding pocket 7 (P7) of the HLA-DR heterodimer, suggesting that these alterations mi

269 ns of FPIR with genetic variants outside the HLA DR-DQ region in the Finnish Type 1 Diabetes Predicti

270 val [95% CI], 1.53 to 2.44), overlapping the HLA locus.

271 ngs implicate not only HLA, particularly the HLA-DQA1 to HLA-DQB1 region, but also the immunoglobulin

272 In the EA population, the HLA-DPB1*13:01 and HLA-DRB1*07:01 alleles were more stro

273 g poses of the abacavir analogues within the HLA-B*57:01 peptide binding groove.

274 Presentation of these HLA-abacavir-peptide complexes to T-cells is hypothesize

275 ith the control of HIV, recognition of these HLA-B57 allomorphs by the killer cell immunoglobulin-lik

276 While this HLA upregulation would seem to be advantageous to the vi

277 5% CI 1.05-11.35, chi-square test) and three HLA alleles (DQB1*06:01, DQA1*05:05 and C*12:02) were id

278 The identification of three HLA-DQ AAs (alpha44, beta57, beta135) conferring T1D ris

279 s demonstrated that EBV peptides can bind to HLA-E and block inhibition of NK cell effector function.

280 ass I or II donor-specific antibody bound to HLA antigens on the donor cell surface in their native c

281 e not only HLA, particularly the HLA-DQA1 to HLA-DQB1 region, but also the immunoglobulin heavy chain

282 85%), and 145 of 205 (71%) developed DSA to HLA-DQ alleles.

283 the NPM1c epitope-HLA-A2 complex but not to HLA-A2 or to HLA-A2 loaded with control peptides.

284 itope-HLA-A2 complex but not to HLA-A2 or to HLA-A2 loaded with control peptides.

285 y: 15% in Europeans) and G-DDF restricted to HLA-DPA1*01:03/DPB1*02:01 and -DPA1*01:03/DPB1*04:01 (al

286 FYQSTCSAVSKGYL (F-EFY) epitope restricted to HLA-DR4, -DR9, and -DR11 (combined allelic frequency: 15

287 o confer different affinities via a variable HLA-C contact, generating an oligoclonal response.

288 linear, multifactorial relationship in which HLA risk alleles are one factor.

289 and processing to the derived adducts) with HLA proteins that present the drug-peptide complex to T

290 ymphomas; these cancers were associated with HLA class I region only and HLA class II region only, im

291 However, AT1R antibodies combined with HLA DSA in patients with active allograft dysfunction we

292 ed in HLA-E(high) Jurkat cells compared with HLA-E(low) Jurkat cells, consistent with higher rates of

293 show that NKG2C(pos) NK cells interact with HLA-E(high) CD8 T cells, which may negatively regulate t

294 month-old DIABIMMUNE study participants with HLA susceptibility to type 1 diabetes were collected.

295 d eplets (VerEp) mismatch was performed with HLA-matchmaker 2.1 version.

296 splantation and may act synergistically with HLA donor-specific antibodies (DSA).

297 dies to 4/18 non-HLA antigens synergize with HLA donor-specific antibodies and significantly increase

298 from these additional factors together with HLA-binding properties by using machine-learning algorit

299 ly diagnosed patients, aged 3-21 years, with HLA-A*02.01+ and H3.3K27M+ status were enrolled in strat

300 ESW utilization was 20.4%, with more zero HLA mismatch (8% vs 4%), living donors (26% vs 20%), and