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

1 to confirm DSAs' specificity for allo-major histocompatibility complex.

2 arkinson's disease with alleles of the major histocompatibility complex.

3 ibility complex-1 tail, and subsequent major histocompatibility complex-1 downregulation and immune e

4 1 subunit of adaptor protein 1 and the major histocompatibility complex-1 tail, and subsequent major

5 hen the tumour and host share the same major histocompatibility complex alleles, the most potent dete

6 n of Parkinson's disease with specific major histocompatibility complex alleles.

7 responses upon antigen presentation by major histocompatibility complex and cognate alphabeta T cell

8 Polymorphisms related to the major histocompatibility complex and interferon (IFN)-gamma ge

9 he transmembrane complexes between the major histocompatibility complex and the T cell receptor (Sign

10 ignals of selection at lactase and the major histocompatibility complex, and in favor of blond hair a

11 numerous sites, often on incompatible major histocompatibility complex, and occurs in the context of

12 ree-way interaction among antigen, the major histocompatibility complex, and the T cell receptor.

13 ody-mediated TRALI induced by the anti-major histocompatibility complex antibody 34-1-2s.

14 s genetics, we performed genotyping of major histocompatibility complex-borne microsatellites and HLA

15 ol region (chromosome 5q31.1), and the major histocompatibility complex (chromosome 6p21-22).

16 iable nature of this protein, a common major histocompatibility complex class (MHC-II) epitope was id

17 a2-microglobulin (B2M), a component of major histocompatibility complex class 1 (MHC I) molecules, as

18 ypes for their ability to downregulate major histocompatibility complex class A (MHC-A) and MHC-B fro

19 markedly more effective at suppressing major histocompatibility complex class I (MHC I) display on th

20 lls depends on antigen presentation by major histocompatibility complex class I (MHC I) molecules.

21 Major histocompatibility complex class I (MHC I) positive sele

22 Certain major histocompatibility complex class I (MHC-I) alleles (e.g.

23 d chaperone facilitating maturation of major histocompatibility complex class I (MHC-I) and the antiv

24 expectedly and uniquely degraded Nef's major histocompatibility complex class I (MHC-I) downregulator

25 35A) bearing a mutation in the cognate major histocompatibility complex class I (MHC-I) epitope that

26 The NLR family member NLRC5 regulates major histocompatibility complex class I (MHC-I) expression du

27 ow cytometry analyses showed decreased major histocompatibility complex class I (MHC-I) expression in

28 ivating mutations that lead to loss of major histocompatibility complex class I (MHC-I) expression.

29 Peptide loading of major histocompatibility complex class I (MHC-I) molecules is

30 at modulate cell surface expression of major histocompatibility complex class I (MHC-I) molecules: th

31 S5 were also elicited, as evidenced by major histocompatibility complex class I (MHC-I) tetramer stai

32 ecules involved in these events is the Major Histocompatibility Complex class I (MHC-I), responsible

33 kill SIV-infected CD4(+) T cells in an major histocompatibility complex class I (MHC-I)-dependent man

34 NKR-P1B:Clr-b interaction represents a major histocompatibility complex class I (MHC-I)-independent m

35 ects with ALS reduce the expression of major histocompatibility complex class I (MHCI) molecules on M

36 Major histocompatibility complex class I (MHCI) proteins have

37 immunity is the recognition of peptide-major histocompatibility complex class I (p-MHC I) proteins di

38 eraction affinity with cognate peptide-major histocompatibility complex class I (pMHCI).

39 mononuclear cell DEGs associated with major histocompatibility complex class I and natural killer ce

40 l immunoglobulin-like receptors (KIR), major histocompatibility complex class I chain-related genes (

41 e, the identification of antigens with major histocompatibility complex class I epitopes is a crucial

42 Major histocompatibility complex class I expression on MDSCs w

43 es of perifascicular fiber atrophy and major histocompatibility complex class I expression.

44 ceptor (iKIR) for which the respective major histocompatibility complex class I ligand is absent on l

45 enerating peptides that could serve as major histocompatibility complex class I ligands, marking cell

46 Major histocompatibility complex class I molecules (MHC I) hel

47 the interaction of Ly49 receptors with major histocompatibility complex class I molecules (MHC-I).

48 owth of melanoma cell lines expressing major histocompatibility complex class I molecules at high lev

49 tudy, we evaluated the contribution of major histocompatibility complex class I molecules to brain at

50 reticulum and subsequent loading onto major histocompatibility complex class I molecules to trigger

51 Major histocompatibility complex class I polypeptide-related s

52 iveness requires positive selection on major histocompatibility complex class I-associated peptides p

53 bacterial metabolites presented by the major histocompatibility complex class I-related molecule MR1.

54 n led to loss of surface expression of major histocompatibility complex class I.

55 with peptides bound to the polymorphic major histocompatibility complex class Ia (MHC-Ia) and class I

56 aracterized by increased expression of major histocompatibility complex class II (approximately 2.0-f

57 loped a mouse strain that lacks murine major histocompatibility complex class II (MHC II) and instead

58 oculation with M. canis also decreased major histocompatibility complex class II (MHC-II) antigen exp

59 Mtb has been reported to block major histocompatibility complex class II (MHC-II) antigen pre

60 TA) is essential for the expression of major histocompatibility complex class II (MHC-II) genes; howe

61 Major histocompatibility complex class II (MHC-II) molecules a

62 Major histocompatibility complex class II (MHC-II) molecules p

63 sentation in addition to the classical major histocompatibility complex class II (MHC-II) peptide pre

64 or mouse CMV (MCMV) epitopes and use a major histocompatibility complex class II (MHC-II) tetramer to

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

66 s antigen-specific CD4(+) T cells in a major histocompatibility complex class II (MHC-II; HLA-DR)-dep

67 A polymorphism at beta57 in some major histocompatibility complex class II (MHCII) alleles of r

68 alpha-syn fibrils, with attenuation of major histocompatibility complex class II (MHCII) and proinfla

69 id cell (ILC3)-intrinsic expression of major histocompatibility complex class II (MHCII) is regulated

70 The major histocompatibility complex class II (MHCII) is ubiquitin

71 DC-to-MC molecule transfers including major histocompatibility complex class II (MHCII) proteins ena

72 une-disease-relevant peptides bound to major histocompatibility complex class II (pMHCII) molecules t

73 en naive CD4(+) T cells engage peptide+major histocompatibility complex class II and co-stimulatory m

74 th AZD1480 inhibited alpha-SYN-induced major histocompatibility complex Class II and inflammatory gen

75 is a superantigen that cross-links the major histocompatibility complex class II and specific V-beta

76 x) to induce infertility in mice whose major histocompatibility complex class II antigen was replaced

77 epitopes that are predicted to be good major histocompatibility complex class II binders and at the s

78 Major histocompatibility complex class II binding and T-cell r

79 ing class II transactivator attenuates major histocompatibility complex class II expression on endoth

80 two transcription factors dedicated to major histocompatibility complex class II expression, suggesti

81 antigen processing rather than peptide-major histocompatibility complex class II loading.

82 We used major histocompatibility complex class II mismatched C57BL/6N

83 had stronger myocardial expression of major histocompatibility complex class II molecule and enhance

84 ng a high density of peptides bound to major histocompatibility complex class II molecules (pMHC) are

85 d the presentation of self antigens by major histocompatibility complex class II molecules in an infl

86 Wild-type LCs upregulated major histocompatibility complex class II molecules, migrated

87 ernalized antigens in combination with major histocompatibility complex class II molecules.

88 ely 30-50%) in expression of CD11b and major histocompatibility complex class II on both monocytes an

89 Furthermore, silencing of major histocompatibility complex class II reduces allogeneic T

90 of VZV-specific CD4(+) T cells with an major histocompatibility complex class II tetramer (epitope of

91 Direct ex vivo staining with peptide-major histocompatibility complex class II tetramers enabled co

92 d formation of the SEB.T-cell receptor.major histocompatibility complex class II trimer.

93 Moreover, the number of mast cells, major histocompatibility complex class II+, or CD11b+ immunocy

94 Major histocompatibility complex class II, a marker of microgl

95 factor, and intragraft transcripts for major histocompatibility complex class II, Toll-like receptors

96 oss-link the T cell receptor (TCR) and major histocompatibility complex class II, triggering a massiv

97 restoration of mature macrophages and major histocompatibility complex class II-expressing dendritic

98 MO2, CD58, and stromal-1-signature and major histocompatibility complex class II-signature genes, whi

99 cated on 6p22.1, and covering lncRNAs (major histocompatibility complex, class I, A (HLA-A) and HLA c

100 ion expression of inflammatory markers major histocompatibility complex-class II and IL6, lesion matr

101 Major histocompatibility complex E (MHC-E) is a highly conserv

102 classically used exosome markers, like major histocompatibility complex, flotillin, and heat-shock 70

103 e-mapping of challenging regions, e.g. major histocompatibility complex for schizophrenia.

104 and expertly curates sequences of the major histocompatibility complex from non-human species and pr

105 d highly (Balb/c in C57BL/6) stringent major histocompatibility complex fully mismatched mouse models

106 non-human leukocyte antigen genes of 3 major histocompatibility complex gene classes but not at allel

107 ry receptor, ATP-binding cassette, and major histocompatibility complex genes.

108 y present survivin peptides on class I major histocompatibility complex, had significantly diminished

109 icates, independent of a specific host major histocompatibility complex haplotype.

110 ies to provide 100 completely resolved major histocompatibility complex haplotypes and to resolve maj

111 Those results revealed two major histocompatibility complex haplotypes associated with sy

112 al localization of DCs specialized for major histocompatibility complex I (MHC I) and MHC II presenta

113 t mice, patient cells showed increased major histocompatibility complex I expression and most CD8(+)

114 High target peptide-major histocompatibility complex-I (pMHC) affinity and T cell

115 he peptides that bind to non-classical major histocompatibility complex Ib Qa-1 molecules and are rec

116 tumour neo-antigens in the context of major histocompatibility complex II (MHCII) are highly desirab

117 lonal stimulation, and displayed lower major histocompatibility complex II expression by antigen-pres

118 d lysosome tubulation and secretion of major histocompatibility complex II in macrophages and dendrit

119 Major histocompatibility complex II tetramers corresponding to

120 creased number of microglia expressing major histocompatibility complex II.

121 ts, resident cardiac MHCII(LO)CCR2(-) (major histocompatibility complex II/C-C motif chemokine recept

122 ctly or related to the function of the Major Histocompatibility Complex in a number of different spec

123 vestigate the plasticity of a class II major histocompatibility complex in the absence of a bound pep

124 evidence that genetic variation in the major histocompatibility complex influences MZL susceptibility

125 Continuous contact with self-major histocompatibility complex ligands is essential for the

126 sented by the evolutionarily conserved major histocompatibility complex-like molecule MR1.

127 To elucidate major histocompatibility complex-linked systemic sclerosis gen

128 ormative clinically relevant RIC mouse major histocompatibility complex-matched alloHCT model by a pr

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

130 ukocytes (but not the parenchyma) were major histocompatibility complex-matched to the recipients (n

131 (P < 2.5e-05) vGWAS signals within the major histocompatibility complex (MHC) across all three study

132 primary Sjogren's syndrome (pSS) with Major Histocompatibility Complex (MHC) alleles is quintessenti

133 Regarding the major histocompatibility complex (MHC) and coevolution, three

134 hood of neoantigen presentation by the major histocompatibility complex (MHC) and subsequent recognit

135 in constructs were transplanted across major histocompatibility complex (MHC) barriers in a porcine a

136 F3 downregulates expression of surface major histocompatibility complex (MHC) class I and class II mo

137 s tumour antigen peptides presented by major histocompatibility complex (MHC) class I and class II mo

138 ) maturation, as well as inhibition of major histocompatibility complex (MHC) class I and class II.

139 The direct major histocompatibility complex (MHC) class I antigen present

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

141 obulin-like receptors (KIRs) and their major histocompatibility complex (MHC) class I ligands.

142 Individuals expressing the major histocompatibility complex (MHC) class I molecule HLA-A2

143 Major histocompatibility complex (MHC) class I molecules deter

144 methods predicting peptide binding to major histocompatibility complex (MHC) class I molecules have

145 ion of peptides that were presented on major histocompatibility complex (MHC) class I molecules in an

146 receptors, many of which interact with major histocompatibility complex (MHC) class I molecules.

147 , are presented at the cell surface by major histocompatibility complex (MHC) class I molecules.

148 exogenous antigens to T cells via both major histocompatibility complex (MHC) class I pathways and MH

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

150 cells also had decreased expression of major histocompatibility complex (MHC) class I proteins, a hal

151 otein signaling, and downregulation of major histocompatibility complex (MHC) class I surface express

152 sitive patients analyzed by performing major histocompatibility complex (MHC) class I tetramer enrich

153 ls is characteristically restricted by major histocompatibility complex (MHC) class I, although rare

154 r cells express multiple receptors for major histocompatibility complex (MHC) class I, including the

155 early inducible-1 (Rae-1) in mice and major histocompatibility complex (MHC) class I-chain-related A

156 ognize lipid antigens presented by the major histocompatibility complex (MHC) class I-like molecule,

157 G2DLs) are a group of stress-inducible major histocompatibility complex (MHC) class I-like molecules

158 Innate variant TFH cells required major histocompatibility complex (MHC) class I-like signaling

159 type of proteasome destined to improve major histocompatibility complex (MHC) class I-mediated antige

160 This study investigated the role of major histocompatibility complex (MHC) class I-related chain A

161 bacterial riboflavin presented by the major histocompatibility complex (MHC) class I-related molecul

162 rrent strategies use genes that encode major histocompatibility complex (MHC) class I-restricted T-ce

163 sin-related protein TAPBPR is a second major histocompatibility complex (MHC) class I-specific chaper

164 model, we found that the expression of major histocompatibility complex (MHC) class II and CD74 in B

165 Suppression of major histocompatibility complex (MHC) class II antigen presen

166 ools of dengue virus-derived predicted major histocompatibility complex (MHC) class II binding peptid

167 guished CD4(+) T cells selected by the major histocompatibility complex (MHC) class II molecule I-A(g

168 es antigenic peptides for loading onto major histocompatibility complex (MHC) class II molecules.

169 show that antigen presentation within major histocompatibility complex (MHC) class II of donor dendr

170 Recently, major histocompatibility complex (MHC) class II tetramers have

171 ation, including the gene encoding the major histocompatibility complex (MHC) class II transactivator

172 Because major histocompatibility complex (MHC) class II(+) cells are m

173 e basis of their expression levels and major histocompatibility complex (MHC) class II-binding capaci

174 mphocytes to be targeted by a panel of major histocompatibility complex (MHC) class II-matched CD4(+)

175 s, CD11b(+) myeloid-derived cells, and major histocompatibility complex (MHC) class II-positive antig

176 renal infiltration with ED1 (CD68) or major histocompatibility complex (MHC) class II-positive cells

177 a complementary approach, we generated major histocompatibility complex (MHC) class II-restricted T c

178 Also, individuals with locally rare major histocompatibility complex (MHC) class IIb genotypes wer

179 The major histocompatibility complex (MHC) contains the most polym

180 ne marrow transplantation (BMT) across major histocompatibility complex (MHC) disparities and may be

181 Genes of the major histocompatibility complex (MHC) encode receptor molecul

182 evious studies have indicated that the major histocompatibility complex (MHC) genes play the most pro

183 que group of animals that have limited major histocompatibility complex (MHC) genetic diversity, such

184 in immunogenicity depends on both host major histocompatibility complex (MHC) genetics and the likeli

185 association with AD risk occurred with major histocompatibility complex (MHC) haplotype A*03:01 B*07:

186 crossreactivity toward multiple other major histocompatibility complex (MHC) haplotypes.

187 The chicken major histocompatibility complex (MHC) has strong genetic asso

188 Disruption of the non-classical Major Histocompatibility Complex (MHC) Ib molecule Qa-1 impair

189 perate simultaneously by analysing the major histocompatibility complex (MHC) in guppies (Poecilia re

190 T cell antigen receptor (TCR)-peptide-major histocompatibility complex (MHC) interface is composed o

191 The Major Histocompatibility Complex (MHC) is a key component of t

192 The binding between a peptide and a major histocompatibility complex (MHC) is one of the most impo

193 Continuous contact with self-major histocompatibility complex (MHC) ligands is essential fo

194 icrosatellite, structural variant, and major histocompatibility complex (MHC) loci, confirming that i

195 The Major Histocompatibility Complex (MHC) locus encodes classical

196 lation level involves variation in the major histocompatibility complex (MHC) locus, but the genes an

197 its feasibility in a clinical setting.Major histocompatibility complex (MHC) matching improves graft

198 rates cGVHD in multiple models: a full major histocompatibility complex (MHC) mismatch model of multi

199 ance of heart allografts across a full major histocompatibility complex (MHC) mismatch.

200 Evidence is mounting that the major histocompatibility complex (MHC) molecule HLA-F (human l

201 otype encoding the HLA-C*08:02 class I major histocompatibility complex (MHC) molecule.

202 gen when presented in the context of a major histocompatibility complex (MHC) molecule.

203 tor (TCR) and peptide presented by the major histocompatibility complex (MHC) molecule.

204 rotein antigens on the cell surface by major histocompatibility complex (MHC) molecules coordinates v

205 and antigenic peptide in complex with major histocompatibility complex (MHC) molecules is a crucial

206 eta T cell receptor (TCR) with peptide-major histocompatibility complex (MHC) molecules on antigen-pr

207 spond to peptide epitopes presented by major histocompatibility complex (MHC) molecules.

208 e interacts with peptides presented by major histocompatibility complex (MHC) molecules.

209 nd was largely restricted by classical major histocompatibility complex (MHC) molecules.

210 Here we use peptide-major histocompatibility complex (MHC) multimers labeled with

211 Major Histocompatibility Complex (MHC) or Human Leukocyte Anti

212 table to either a TCR focus on exposed major histocompatibility complex (MHC) polymorphisms or the de

213 Sequence-based analyses of major histocompatibility complex (MHC) polymorphisms reveal ex

214 that was dependent on the nonclassical major histocompatibility complex (MHC) protein CD1d, which pre

215 e response process is regulated by the major histocompatibility complex (MHC) protein which is encode

216 th which complexes of self peptide and major histocompatibility complex (MHC) proteins are recognized

217 s reactive to complexes of peptide and major histocompatibility complex (MHC) proteins, many other ty

218 ants expanding throughout the extended major histocompatibility complex (MHC) region and 68 non-LS-as

219 The mammalian Major Histocompatibility Complex (MHC) region contains several

220 Multiple single variants within the major histocompatibility complex (MHC) region were observed to

221 influenced by genetic variation in the major histocompatibility complex (MHC) region.

222 88) for HPV8 seropositivity within the major histocompatibility complex (MHC) region.

223 ith the strongest association from the major histocompatibility complex (MHC) region.

224 sociations, in the IL28B/IFNL4 and the major histocompatibility complex (MHC) regions, with spontaneo

225 Major histocompatibility complex (MHC) restriction is a fundam

226 Major histocompatibility complex (MHC) restriction is a unique

227 t mapping, independent localization of major histocompatibility complex (MHC) risk from classical HLA

228 ere up to 94.4% pure, as determined by major histocompatibility complex (MHC) tetramer analysis.

229 ange for complexes of self-peptide and major histocompatibility complex (MHC) undergo positive select

230 uding the tumor necrosis factor (TNF), major histocompatibility complex (MHC), interleukin 23 recepto

231 ve been implicated in vertebrates: the major histocompatibility complex (MHC), which could be vertebr

232 ecipients, most prominently within the major histocompatibility complex (MHC), which encodes human le

233 Despite the availability of major histocompatibility complex (MHC)-binding peptide predict

234 Here we identified 107 major histocompatibility complex (MHC)-bound HIV peptides dire

235 tributed to an absence of cell surface major histocompatibility complex (MHC)-I molecule expression.

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

237 Here we show the efficacy of major histocompatibility complex (MHC)-matched allogeneic neur

238 Our current understanding of major histocompatibility complex (MHC)-mediated antigen presen

239 In a full major histocompatibility complex (MHC)-mismatched, multiorgan

240 rate diverse T cell subsets, including major histocompatibility complex (MHC)-restricted alphabeta T

241 strong evidence of association to the major histocompatibility complex (MHC).

242 One interesting example is the chicken major histocompatibility complex (MHC).

243 This enrichment was driven by the major histocompatibility complex (MHC).

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

245 odels, have become synonymous with the major histocompatibility complex (MHC).

246 ll selection by sensing the density of major histocompatibility complex (MHC):peptide antigen complex

247 n of IL-12, and inhibition of class II major histocompatibility complex (MHC-II) molecules in infecte

248 The major-histocompatibility-complex-(MHC)-class-I-related molecul

249 rmed in mice across varying degrees of major histocompatibility complex mismatch combinations.

250 himerism model receiving BCNU across a major histocompatibility complex mismatch.

251 in exhibited >100-day survival of full major histocompatibility complex mismatched allografts, wherea

252 We performed major histocompatibility complex mismatched aorta to carotid a

253 went nonmyeloablative conditioning and major histocompatibility complex mismatched BMT with or withou

254 transplants were performed using minor major histocompatibility complex-mismatched B6.C-H2 donor hear

255 Using the major histocompatibility complex-mismatched mouse orthotopic l

256 hyma and the passenger leukocytes were major histocompatibility complex-mismatched to the recipients

257 uti rat and Balb mouse donors to fully major histocompatibility complex-mismatched Wistar Furth rat o

258 dney allograft rejection using a fully major histocompatibility complex-mismatched, life-sustaining,

259 ges a peptide bound to the restricting major histocompatibility complex molecule (pMHC), it transmits

260 foreign peptide antigens presented in major histocompatibility complex molecules (pMHC) is essential

261 ic peptides within class I or class II major histocompatibility complex molecules (pMHCI or pMHCII, r

262 ts to ablate EC expression of class II major histocompatibility complex molecules and with it, the ca

263 Ablation of endothelial cell class II major histocompatibility complex molecules by small interferin

264 gnize peptide antigens associated with major histocompatibility complex molecules expressed on the su

265 s) recognize agonist peptides bound to major histocompatibility complex molecules on antigen-presenti

266 cell responses is complex and involves major histocompatibility complex molecules on transplanted org

267 cessors of antigen for presentation by major histocompatibility complex molecules, recent findings po

268 interleukin-21 and enriched by peptide-major histocompatibility complex multimer-guided cell sorting.

269 ic CD8 T cells were tracked down using major histocompatibility complex multimers against the immunod

270 Of the 110 non-major histocompatibility complex multiple sclerosis-associated

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

272 nel support vector machines to predict major histocompatibility complex-peptide binding.

273 er feature interactions for predicting major histocompatibility complex-peptide binding.

274 ed progressively with lowering peptide major histocompatibility complex (pMHC) affinity.

275 hich T cell receptor (TCR) and peptide major histocompatibility complex (pMHC) interact.

276 is interaction of pre-TCR with peptide-major histocompatibility complex (pMHC) molecules has recently

277 ters its antigenic ligand, the peptide-major histocompatibility complex (pMHC), on the surface of ant

278 sequences using a panel of peptide and major histocompatibility complex (pMHC)-tetramer-sorted cells

279 o functionally engage multiple peptide-major histocompatibility complexes (pMHC) are unclear.

280 th autoimmune disease-relevant peptide-major histocompatibility complexes (pMHC) blunted autoimmune r

281 In searching for peptide-loaded major histocompatibility complexes (pMHCs), they must solve a

282 ctionally engage with multiple peptide-major histocompatibility complexes (pMHCs), we examined the IL

283 through interactions with peptide and major histocompatibility complexes (pMHCs).

284 n antibody specific for human class II major histocompatibility complex products and used it to nonin

285 th the extremely polymorphic nature of major histocompatibility complex products within the species.

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

287 h foreign antigens bound to alleles of major histocompatibility complex proteins (MHC) that they were

288 HLA-A is a class I major histocompatibility complex receptor that presents peptid

289 als for oligoclonal band status in the major histocompatibility complex region for the rs9271640*A-rs

290 Association within the major histocompatibility complex region was also observed in e

291 identify two novel associations in the major histocompatibility complex region with immunoglobulin G

292 MAIT cells, surface expression of the major histocompatibility complex-related protein 1 (MR1), and

293 ing antigen recognition independent of major histocompatibility complex restriction, while retaining

294 Ever since the discovery of the major histocompatibility complex, scientific and clinical unde

295 "A-into-O" transplantation (major histocompatibility complex syngeneic) was modeled by tra

296 amental difference between the CD1 and major histocompatibility complex systems is that all humans ex

297 to infiltration of activated class II major histocompatibility complex(+) T cells.

298 ctors aside from intrinsic TCR-peptide-major histocompatibility complex (TCR-peptide-MHC) reactivity

299 single nucleotide polymorphisms of the major histocompatibility complex to precisely identify risk lo

300 Finally, we observed the expression of major histocompatibility complex type I genes in a subset of a