ライフサイエンスコーパス: major histocompatibility

1 ained by increased recipient mismatching for major histocompatibility antigens or minor histocompatib

2 at enhances pathogenicity by down-regulating major histocompatibility class I (MHC-I) expression to e

3 r enzyme that optimizes the peptide cargo of major histocompatibility class I (MHC-I) molecules and r

4 sed semiallogeneic donor cells mismatched at major histocompatibility class I can enhance tolerance t

5 and the beta-2 microglobulin subunit of the major histocompatibility class I complex (B2M)(3).

6 ance model induced by a single DST across an major histocompatibility class I mismatch in an unmanipu

7 face levels of two different substrates: the major histocompatibility class I molecule HLA-A2 and the

8 +) T cell priming required the expression of major histocompatibility class I molecules by cDC1.

9 In patients, expression of major histocompatibility class II in melanoma is linked

10 ens (SAgs), which engage lateral surfaces of major histocompatibility class II molecules and T-cell r

11 processing by cDC2, as selective deletion of major histocompatibility class II molecules in cDC1 also

12 Furthermore, deletion of either major histocompatibility class II or CD40 in cDC1 impair

13 ion of primary Sjogren's syndrome (pSS) with Major Histocompatibility Complex (MHC) alleles is quinte

14 Variants in major histocompatibility complex (MHC) and in interferon

15 ptors (TCRs) recognize antigens presented by major histocompatibility complex (MHC) and MHC class I-l

16 e antigens bound to molecules encoded by the major histocompatibility complex (MHC) and presented on

17 likelihood of neoantigen presentation by the major histocompatibility complex (MHC) and subsequent re

18 Conformational changes of major histocompatibility complex (MHC) antigens have the

19 n of inhibitory NK cell receptors with their major histocompatibility complex (MHC) class I (or HLA c

20 rogates tumour antigen peptides presented by major histocompatibility complex (MHC) class I and class

21 d human iPSCs lose their immunogenicity when major histocompatibility complex (MHC) class I and II ge

22 ational prediction tools to identify LASV GP major histocompatibility complex (MHC) class I and II T-

23 s of anti-tumor cytolytic activity and lower major histocompatibility complex (MHC) class I gene expr

24 Genetic variability across the three major histocompatibility complex (MHC) class I genes (hu

25 Here we found a central role for major histocompatibility complex (MHC) class I in contro

26 gen class I (HLA-I) molecules are encoded by major histocompatibility complex (MHC) class I loci in h

27 coding a transcription factor that regulates major histocompatibility complex (MHC) class I molecule

28 s long, are presented at the cell surface by major histocompatibility complex (MHC) class I molecules

29 ification of peptides that were presented on major histocompatibility complex (MHC) class I molecules

30 Major Histocompatibility Complex (MHC) class I molecules

31 In SWATH-MS major histocompatibility complex (MHC) class I proteins

32 Peptide antigen presentation by major histocompatibility complex (MHC) class I proteins

33 In comparison to the families of major histocompatibility complex (MHC) class I, MHC clas

34 be presented on the cell surface as part of major histocompatibility complex (MHC) class I, suggesti

35 ously expressed across primary TCLs, whereas major histocompatibility complex (MHC) class I, which ca

36 Mapping studies with major histocompatibility complex (MHC) class I- and clas

37 We identified major histocompatibility complex (MHC) class I-binding e

38 Neonatal Fc-receptor (FcRn), the major histocompatibility complex (MHC) class I-like Fc-r

39 ll targeting of virus-infected cells and the major histocompatibility complex (MHC) class I-primed CD

40 ors of bacterial riboflavin presented by the major histocompatibility complex (MHC) class I-related m

41 ost current strategies use genes that encode major histocompatibility complex (MHC) class I-restricte

42 sponses by enhancing peptide presentation by major histocompatibility complex (MHC) class I.

43 e protein-derived antigens in the context of major histocompatibility complex (MHC) class Ia and clas

44 with pools of dengue virus-derived predicted major histocompatibility complex (MHC) class II binding

45 CD4 T cells and major histocompatibility complex (MHC) class II molecule

46 T cells, even in tumours that do not express major histocompatibility complex (MHC) class II molecule

47 produces antigenic peptides for loading onto major histocompatibility complex (MHC) class II molecule

48 TCR on differentiating CD4(+) T cells or of major histocompatibility complex (MHC) class II on intes

49 IECs constitutively express low levels of major histocompatibility complex (MHC) class II proteins

50 e furthermore find that a variant within the major histocompatibility complex (MHC) class II region c

51 Recently, major histocompatibility complex (MHC) class II tetramer

52 model of chronic typhoid fever combined with major histocompatibility complex (MHC) class II tetramer

53 screen in human cells, we identify that the major histocompatibility complex (MHC) class II transact

54 resentation, including the gene encoding the major histocompatibility complex (MHC) class II transact

55 We exemplify this concept with SIEC major histocompatibility complex (MHC) class II, which i

56 In a complementary approach, we generated major histocompatibility complex (MHC) class II-restrict

57 tation of antigen peptides in the context of major histocompatibility complex (MHC) class II.

58 The major histocompatibility complex (MHC) contains the most

59 y of antigenic peptides displayed in a given major histocompatibility complex (MHC) context.

60 en presenting cells (APCs) with intact donor major histocompatibility complex (MHC) derived from allo

61 ter bone marrow transplantation (BMT) across major histocompatibility complex (MHC) disparities and m

62 Major histocompatibility complex (MHC) genes encode prot

63 Proteins encoded by the classical major histocompatibility complex (MHC) genes incite the

64 h mismatches at half (haploidentical) or all major histocompatibility complex (MHC) genes.

65 a unique group of animals that have limited major histocompatibility complex (MHC) genetic diversity

66 Although allelic diversity at the major histocompatibility complex (MHC) has implications

67 The major histocompatibility complex (MHC) has long served a

68 Generally, this approach is referred to as major histocompatibility complex (MHC) homo-to-hetero tr

69 st evidence for the role of an allele of the major histocompatibility complex (MHC) I gene HLA-B in t

70 ost antigenic peptides that bind stably to a major histocompatibility complex (MHC) I molecule for di

71 The major histocompatibility complex (MHC) is a central comp

72 The Major Histocompatibility Complex (MHC) is a key componen

73 The major histocompatibility complex (MHC) is responsible fo

74 The Major Histocompatibility Complex (MHC) is the most genet

75 strongest common genetic associations in the major histocompatibility complex (MHC) locus, an associa

76 in and its feasibility in a clinical setting.Major histocompatibility complex (MHC) matching improves

77 er been described in the context of multiple major histocompatibility complex (MHC) mismatches.

78 Nonclassical (class-Ib) major histocompatibility complex (MHC) molecules (MHC-Ib

79 Major histocompatibility complex (MHC) molecules are exp

80 sed congenic mice to examine the function of major histocompatibility complex (MHC) molecules in elim

81 -7 (HHV-7) U21 glycoprotein binds to class I major histocompatibility complex (MHC) molecules in the

82 to target cells that present cognate peptide-major histocompatibility complex (MHC) molecules.

83 or endogenous processing and presentation on major histocompatibility complex (MHC) molecules.

84 AnthOligo was tested by capturing the Major Histocompatibility Complex (MHC) of a random sampl

85 he cellular form of the TRA and the class of major histocompatibility complex (MHC) on which antigen

86 on with the proteins of class I and class II major histocompatibility complex (MHC) pathways.

87 ttributable to either a TCR focus on exposed major histocompatibility complex (MHC) polymorphisms or

88 nsion that was dependent on the nonclassical major histocompatibility complex (MHC) protein CD1d, whi

89 immune response process is regulated by the major histocompatibility complex (MHC) protein which is

90 ed binding strengths to class-I and class-II major histocompatibility complex (MHC) proteins for 284

91 dies targeting human leukocyte antigen (HLA)/major histocompatibility complex (MHC) proteins limit su

92 e processed to neo-antigens and presented by major histocompatibility complex (MHC) proteins to T cel

93 ecognize short peptide antigens presented on major histocompatibility complex (MHC) proteins.

94 The mammalian Major Histocompatibility Complex (MHC) region contains s

95 Multiple single variants within the major histocompatibility complex (MHC) region were obser

96 ant associations, in the IL28B/IFNL4 and the major histocompatibility complex (MHC) regions, with spo

97 Major histocompatibility complex (MHC) restriction is a

98 ocus on the recovery of haplotype diversity, major histocompatibility complex (MHC) variants, satelli

99 (CD8 Treg) that recognize the Qa-1 class Ib major histocompatibility complex (MHC), a mouse homolog

100 d immunocompetence via heterozygosity at the major histocompatibility complex (MHC), a widely-used ge

101 tracellular complex comprising a peptide and major histocompatibility complex (MHC), and induce intra

102 The interaction between the class I major histocompatibility complex (MHC), the peptide pres

103 and recipients, most prominently within the major histocompatibility complex (MHC), which encodes hu

104 y we tested whether genetic variation in the major histocompatibility complex (MHC), which is associa

105 We assessed the evidence for major histocompatibility complex (MHC)-based mate prefer

106 is attributed to an absence of cell surface major histocompatibility complex (MHC)-I molecule expres

107 on free peptides or on those bound to their major histocompatibility complex (MHC)-I-presenting mole

108 We now show that major histocompatibility complex (MHC)-II and its master

109 se (GVHD) largely has been extrapolated from major histocompatibility complex (MHC)-matched murine sk

110 Using major histocompatibility complex (MHC)-mismatched and MH

111 In a full major histocompatibility complex (MHC)-mismatched, multi

112 cularly the third CDRs (CDR3s) interact with major histocompatibility complex (MHC)-presented epitope

113 Major histocompatibility complex (MHC)-related 1-restric

114 o generate diverse T cell subsets, including major histocompatibility complex (MHC)-restricted alphab

115 D) due to human T-cell recognition of murine major histocompatibility complex (MHC).

116 f hard to assemble gene clusters such as the major histocompatibility complex (MHC).

117 stinct from interactions between the TCR and major histocompatibility complex (MHC).

118 imal models, have become synonymous with the major histocompatibility complex (MHC).

119 iploid assembly is particularly useful - the Major Histocompatibility Complex (MHC).

120 recognition of antigens presented by class I major histocompatibility complex (MHC-I) proteins on tum

121 T-cell receptor (TCR) with a peptide-loaded major histocompatibility complex (p/MHC) leads to T-cell

122 thin which T cell receptor (TCR) and peptide major histocompatibility complex (pMHC) interact.

123 The natural peptide-major histocompatibility complex (pMHC) ligand for T cel

124 This interaction of pre-TCR with peptide-major histocompatibility complex (pMHC) molecules has re

125 ll receptor (TCR) binding to agonist peptide major histocompatibility complex (pMHC) triggers signali

126 f TCR sequences using a panel of peptide and major histocompatibility complex (pMHC)-tetramer-sorted

127 her factors aside from intrinsic TCR-peptide-major histocompatibility complex (TCR-peptide-MHC) react

128 Mrc1, Retnla, and H2-a/e (encoding class II major histocompatibility complex [MHC] proteins) and man

129 ciation of Parkinson's disease with specific major histocompatibility complex alleles.

130 ne responses by downregulating expression of major histocompatibility complex and interfering with an

131 n of the transmembrane complexes between the major histocompatibility complex and the T cell receptor

132 is performant, flexible and supports several major histocompatibility complex binding affinity predic

133 ning for antigen-reactive TCRs using peptide major histocompatibility complex binding and cellular ac

134 he variable nature of this protein, a common major histocompatibility complex class (MHC-II) epitope

135 M subtypes for their ability to downregulate major histocompatibility complex class A (MHC-A) and MHC

136 the repertoire of peptides presented by the major histocompatibility complex class I (MHC I) is a ke

137 Adaptive immunity vitally depends on major histocompatibility complex class I (MHC I) molecul

138 in different steps during the maturation of major histocompatibility complex class I (MHC I) protein

139 es presented by the evolutionarily conserved major histocompatibility complex class I (MHC I)-related

140 50% of rhesus macaques (RMs) expressing the major histocompatibility complex class I (MHC-I) allele

141 To understand the role of major histocompatibility complex class I (MHC-I) and MHC

142 cently identified specific transactivator of major histocompatibility complex class I (MHC-I) compone

143 Interestingly, CXCL14 expression restores major histocompatibility complex class I (MHC-I) express

144 The NLR family member NLRC5 regulates major histocompatibility complex class I (MHC-I) express

145 Second, polymorphism of the human major histocompatibility complex class I (MHC-I) gene re

146 iment expressed the elite control-associated major histocompatibility complex class I (MHC-I) molecul

147 efficiently presented in the context of the major histocompatibility complex class I (MHC-I) molecul

148 Tumors frequently subvert major histocompatibility complex class I (MHC-I) peptide

149 c CD8(+) T cell responses were documented by major histocompatibility complex class I (MHC-I) tetrame

150 y mutations or loss of heterozygosity of the major histocompatibility complex class I (MHC-I), which

151 are needed to identify peptides presented by major histocompatibility complex class I (MHC-I).

152 ature antigenic peptides for presentation by major histocompatibility complex class I (MHCI) molecule

153 iated immunity is the recognition of peptide-major histocompatibility complex class I (p-MHC I) prote

154 Peptide-loaded major histocompatibility complex class I (pMHC-I) molecu

155 ific CD8(+) T cells, applying peptide-loaded major histocompatibility complex class I (pMHCI) tetrame

156 tained the ability to induce upregulation of major histocompatibility complex class I antigen express

157 he cytosol, where they access the endogenous major histocompatibility complex class I antigen process

158 neurons by preventing their up-regulation of major histocompatibility complex class I antigen, thus p

159 Major histocompatibility complex class I chain-related (

160 8 T cells targeting dominant and subdominant major histocompatibility complex class I epitopes prolif

161 dition, sorafenib was found to down-regulate major histocompatibility complex class I expression of t

162 ways and frequent B2M alterations that limit major histocompatibility complex class I expression, as

163 Major histocompatibility complex class I molecules (MHC

164 this study, we evaluated the contribution of major histocompatibility complex class I molecules to br

165 tumours that have lost surface expression of major histocompatibility complex class I molecules.

166 ncorporating proximal variant correction for major histocompatibility complex class I neoantigen pept

167 ctural analysis shows FcRn is a nonclassical major histocompatibility complex Class I receptor, which

168 ons between SNPs and VL were observed in the major histocompatibility complex class I region (MHC I),

169 albumin, as well as a viral peptide-specific major histocompatibility complex class I tetramer, we in

170 eptide-MHC-I complex (where MHC-I represents major histocompatibility complex class I).

171 nodes (LNs), but not in the spleen, through major histocompatibility complex class I-dependent inter

172 between the hyperactive ERBB-STAT3 axis and major histocompatibility complex class I-mediated tumor

173 epitopes (amino acids 11-30 and 41-60) and 1 major histocompatibility complex class I-restricted epit

174 ine H2-O) is a highly conserved nonclassical major histocompatibility complex class II (MHC II) acces

175 enting antigenic peptides to CD4(+) T cells, major histocompatibility complex class II (MHC II) also

176 The major histocompatibility complex class II (MHC II)-CD4 i

177 aled alterations in both the CD11c(+) DC and major histocompatibility complex class II (MHC)-II(+) ma

178 AG-3) is an immune inhibitory receptor, with major histocompatibility complex class II (MHC-II) as a

179 genome-wide CRISPR-Cas9 screening, that the major histocompatibility complex class II (MHC-II) human

180 Major histocompatibility complex class II (MHC-II) molec

181 f-peptides displayed by a defined autoimmune major histocompatibility complex class II (MHC-II) molec

182 ncodes the beta subunit of the non-classical major histocompatibility complex class II (MHC-II)-like

183 ologous antigen-specific CD4(+) T cells in a major histocompatibility complex class II (MHC-II; HLA-D

184 -DM (HLA-DM) is an integral component of the major histocompatibility complex class II (MHCII) antige

185 ia and that presentation of such antigens on major histocompatibility complex class II (MHCII) leads

186 erantigens to T cell receptors (TCRs) and/or major histocompatibility complex class II (MHCII) molecu

187 ate in DC-to-MC molecule transfers including major histocompatibility complex class II (MHCII) protei

188 cell effector responses during infection was major histocompatibility complex class II (MHCII)-depend

189 emoval of the complex of cognate peptide and major histocompatibility complex class II (pMHCII) from

190 Accessory molecules (major histocompatibility complex class II [MHC-II], CD80

191 ore, antibiotic-induced broad suppression of major histocompatibility complex class II antigen presen

192 UW-3/Cx) to induce infertility in mice whose major histocompatibility complex class II antigen was re

193 nduced deaminase, and immune evasion through major histocompatibility complex class II downregulation

194 nes in peripheral T-cell counts, and reduced major histocompatibility complex class II expression lev

195 pleen's weight, a lymphopenia, a decrease of major histocompatibility complex class II expression on

196 targeting class II transactivator attenuates major histocompatibility complex class II expression on

197 ased CD4 T-cell counts and downregulation of major histocompatibility complex class II expression on

198 also downregulation of the FCER2, CD52, and major histocompatibility complex class II genes.

199 We used major histocompatibility complex class II mismatched C57

200 teria, had stronger myocardial expression of major histocompatibility complex class II molecule and e

201 esenting a high density of peptides bound to major histocompatibility complex class II molecules (pMH

202 In spleen, an increased expression of major histocompatibility complex class II molecules on d

203 degraded, and the peptides are presented on major histocompatibility complex class II molecules, the

204 s are bacterial superantigens, which bind to major histocompatibility complex class II on antigen-pre

205 oximately 30-50%) in expression of CD11b and major histocompatibility complex class II on both monocy

206 ctivate T-cell-dependent immune responses by major histocompatibility complex class II presentation.

207 HCV-specific CD4(+) T-cell populations using major histocompatibility complex class II tetramers in v

208 rmore, MIA microglia increased expression of major histocompatibility complex class II that was coupl

209 rovide the first demonstration that not only major histocompatibility complex class II, but also clas

210 The major histocompatibility complex class-I (MHC-I) peptide

211 usly shown to be TAAs, their presentation on major histocompatibility complex classes I (MHC-I) and I

212 Major histocompatibility complex E (MHC-E) is a highly c

213 cells in solid tumors, HRSCs frequently lack major histocompatibility complex expression, and the mec

214 llects and expertly curates sequences of the major histocompatibility complex from non-human species

215 /c) and highly (Balb/c in C57BL/6) stringent major histocompatibility complex fully mismatched mouse

216 is highly specific and dependent on the host major histocompatibility complex genotype.

217 The major histocompatibility complex haplotype represents th

218 ssemblies to provide 100 completely resolved major histocompatibility complex haplotypes and to resol

219 Those results revealed two major histocompatibility complex haplotypes associated w

220 erential localization of DCs specialized for major histocompatibility complex I (MHC I) and MHC II pr

221 ase 1 (ERAP1) and ERAP2 critically shape the major histocompatibility complex I (MHC I) immunopeptido

222 s and macrophages acquire memory specific to major histocompatibility complex I (MHC-I) antigens, and

223 monstrated to epigenetically reverse the low major histocompatibility complex I expression caused by

224 on by T cells owing to the downregulation of major histocompatibility complex I surface expression.

225 gulated, consequently resulting in increased major histocompatibility complex I surface expression.

226 Major histocompatibility complex II (MHC II) molecules a

227 hes phagosomal tubule formation, and impairs major histocompatibility complex II (MHC-II) presentatio

228 ed with circulating neutrophils, with higher major histocompatibility complex II (MHCII) expression,

229 -permitting H2s or disease-nonpermitting H2b major histocompatibility complex II haplotypes.

230 atherosclerosis, we used a novel tetramer of major histocompatibility complex II to track T cells rea

231 y T cell differentiation, prolonged monocyte major histocompatibility complex II upregulation and per

232 These results indicate that major histocompatibility complex II-associated susceptib

233 subsets, resident cardiac MHCII(LO)CCR2(-) (major histocompatibility complex II/C-C motif chemokine

234 uM) comparable to many alphabeta TCR-peptide major histocompatibility complex interactions.

235 rogate peptides derived from a yeast peptide major histocompatibility complex library of some of the

236 s, targeting the BRCA1 gene, the entire 4-Mb major histocompatibility complex locus and 18 well-chara

237 ablished skin transplant model with a single major histocompatibility complex mismatch, we compared t

238 underwent nonmyeloablative conditioning and major histocompatibility complex mismatched BMT with or

239 Using multimers of peptide major histocompatibility complex molecules (pMHC) and of

240 aVbeta module to recognize peptides bound to major histocompatibility complex molecules (pMHCs) in "v

241 nize the same antigenic peptide presented on major histocompatibility complex molecules but experienc

242 Ablation of endothelial cell class II major histocompatibility complex molecules by small inte

243 t recognize peptide antigens associated with major histocompatibility complex molecules expressed on

244 olerant and restricted to the recognition of major histocompatibility complex molecules presenting pe

245 as processors of antigen for presentation by major histocompatibility complex molecules, recent findi

246 ed linked SNPs in distinct blocks within the major histocompatibility complex on 6p21.

247 and upregulation of class I molecules of the major histocompatibility complex on tumour cells.

248 unological tolerance by down-regulating both major histocompatibility complex pathways (MHC I and II)

249 -domain antibody specific for human class II major histocompatibility complex products and used it to

250 ope with the extremely polymorphic nature of major histocompatibility complex products within the spe

251 (HLA)-DQ2.5 (DQA1*05/DQB1*02) is a class-II major histocompatibility complex protein associated with

252 agonist peptides are presented to the TCR by major histocompatibility complex proteins expressed by a

253 system by trimming peptides for loading onto major histocompatibility complex proteins.

254 TNF signaling, psoriasis pathology, and the major histocompatibility complex region.

255 athogenic SIV challenge virus, non-canonical major histocompatibility complex restriction, and absent

256 469 located on 6p22.1, and covering lncRNAs (major histocompatibility complex, class I, A (HLA-A) and

257 poietin 2; myeloperoxidase; lactoperoxidase; major histocompatibility complex, class I, A; major hist

258 bility complex, class II, isotype DR beta I; major histocompatibility complex, class I, C; and major

259 histocompatibility complex, class I, C; and major histocompatibility complex, class II, isotype DQ b

260 ajor histocompatibility complex, class I, A; major histocompatibility complex, class II, isotype DR b

261 e associated with expression of genes in the major histocompatibility complex, including C4A and C4B,

262 UC-MSC) that present low antigenicity (i.e., major histocompatibility complex, MHC).

263 Ever since the discovery of the major histocompatibility complex, scientific and clinica

264 Register, three in the Dunedin study) in the major histocompatibility complex, which were associated

265 compatibility complex-1 tail, and subsequent major histocompatibility complex-1 downregulation and im

266 the mu1 subunit of adaptor protein 1 and the major histocompatibility complex-1 tail, and subsequent

267 However, the mechanisms by which major histocompatibility complex-associated genetic susc

268 lerosis genetics, we performed genotyping of major histocompatibility complex-borne microsatellites a

269 ed lesion expression of inflammatory markers major histocompatibility complex-class II and IL6, lesio

270 IL-6 leads to long-term (>75 d) survival of major histocompatibility complex-different skin allograf

271 mmunotherapies fail to exploit their in situ major histocompatibility complex-independent tumoricidal

272 To elucidate major histocompatibility complex-linked systemic scleros

273 an informative clinically relevant RIC mouse major histocompatibility complex-matched alloHCT model b

274 We investigated a murine model of major histocompatibility complex-matched multiple minor

275 ffect of Notch-1 receptor inhibition in full major histocompatibility complex-mismatch murine cardiac

276 is a fundamental metric of diversity at the major histocompatibility complex-peptide complex, which

277 ognize antigens presented on non-polymorphic major histocompatibility complex-related 1 (MR1) molecul

278 ope overlapped with the binding site for the major histocompatibility complex.

279 n of Parkinson's disease with alleles of the major histocompatibility complex.

280 ion of random self-peptides presented on the major histocompatibility complex.

281 ily target peptide antigens presented by the major histocompatibility complex.

282 To perform detailed fine-mapping of the major-histocompatibility-complex region, we conducted ne

283 The major-histocompatibility-complex-(MHC)-class-I-related m

284 d production of recombinant patient-specific major histocompatibility complexes (MHC) loaded with the

285 Peptides bound to class I major histocompatibility complexes (MHC) play a critical

286 ing antigenic peptides presented by class II major histocompatibility complexes (MHC-II).

287 Peptide binding to major histocompatibility complexes (MHCs) is a central c

288 ional modeling of peptide display by class I major histocompatibility complexes (MHCs) is essential f

289 ted with autoimmune disease-relevant peptide-major histocompatibility complexes (pMHC) blunted autoim

290 are presented as processed peptides bound to major histocompatibility complexes (pMHC).

291 In searching for peptide-loaded major histocompatibility complexes (pMHCs), they must so

292 to functionally engage with multiple peptide-major histocompatibility complexes (pMHCs), we examined

293 ignals of African ancestry enrichment at the major histocompatibility locus on chromosome 6, consiste

294 e identity bound to both dendritic cell (DC) major histocompatibility (MHC) class I and MHC class II-

295 is dependent on CD103(+) dendritic cells and major histocompatibility (MHC) class Ia molecules.

296 We have reported that the major histocompatibility molecule HLA-DQ2 (DQA1*05:01/DQ

297 urpose, we employ synTacs, which are dimeric major histocompatibility molecule scaffolds of defined c

298 ne system's ability to recognize peptides on major histocompatibility molecules contributes to the er

299 enic lymphocytes, and utilization of peptide-major histocompatibility multimers, along with imaging t

300 PCSK9 antibodies-increases the expression of major histocompatibility protein class I (MHC I) protein