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

1 erlapped with the binding site for the major histocompatibility complex.

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

3 random self-peptides presented on the major histocompatibility complex.

4 rget peptide antigens presented by the major histocompatibility complex.

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

6 1 subunit of adaptor protein 1 and the major histocompatibility complex-1 tail, and subsequent major

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

8 ponses by downregulating expression of major histocompatibility complex and interfering with antigen

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

10 However, the mechanisms by which major histocompatibility complex-associated genetic susceptibi

11 formant, flexible and supports several major histocompatibility complex binding affinity prediction t

12 or antigen-reactive TCRs using peptide major histocompatibility complex binding and cellular activati

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

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

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

16 epertoire of peptides presented by the major histocompatibility complex class I (MHC I) is a key step

17 Adaptive immunity vitally depends on major histocompatibility complex class I (MHC I) molecules loa

18 fferent steps during the maturation of major histocompatibility complex class I (MHC I) proteins, fro

19 sented by the evolutionarily conserved major histocompatibility complex class I (MHC I)-related molec

20 f rhesus macaques (RMs) expressing the major histocompatibility complex class I (MHC-I) allele Mamu-B

21 To understand the role of major histocompatibility complex class I (MHC-I) and MHC-II in

22 identified specific transactivator of major histocompatibility complex class I (MHC-I) component gen

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

24 erestingly, CXCL14 expression restores major histocompatibility complex class I (MHC-I) expression on

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

26 iently presented in the context of the major histocompatibility complex class I (MHC-I) molecule H-2-

27 expressed the elite control-associated major histocompatibility complex class I (MHC-I) molecule Mamu

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

29 +) T cell responses were documented by major histocompatibility complex class I (MHC-I) tetramer stai

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

31 tions or loss of heterozygosity of the major histocompatibility complex class I (MHC-I), which has be

32 eded to identify peptides presented by major histocompatibility complex class I (MHC-I).

33 antigenic peptides for presentation by major histocompatibility complex class I (MHCI) molecules and

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

35 Peptide-loaded major histocompatibility complex class I (pMHC-I) molecules ar

36 D8(+) T cells, applying peptide-loaded major histocompatibility complex class I (pMHCI) tetramer tech

37 the ability to induce upregulation of major histocompatibility complex class I antigen expression, b

38 osol, where they access the endogenous major histocompatibility complex class I antigen processing pa

39 s by preventing their up-regulation of major histocompatibility complex class I antigen, thus preserv

40 Major histocompatibility complex class I chain-related (MIC) A

41 lls targeting dominant and subdominant major histocompatibility complex class I epitopes proliferated

42 , sorafenib was found to down-regulate major histocompatibility complex class I expression of tumor c

43 nd frequent B2M alterations that limit major histocompatibility complex class I expression, as in cHL

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

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

46 s that have lost surface expression of major histocompatibility complex class I molecules.

47 rating proximal variant correction for major histocompatibility complex class I neoantigen peptides,

48 analysis shows FcRn is a nonclassical major histocompatibility complex Class I receptor, which is em

49 tween SNPs and VL were observed in the major histocompatibility complex class I region (MHC I), with

50 n, as well as a viral peptide-specific major histocompatibility complex class I tetramer, we interrog

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

52 (LNs), but not in the spleen, through major histocompatibility complex class I-dependent interaction

53 en the hyperactive ERBB-STAT3 axis and major histocompatibility complex class I-mediated tumor immuno

54 es (amino acids 11-30 and 41-60) and 1 major histocompatibility complex class I-restricted epitope (a

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

56 -O) is a highly conserved nonclassical major histocompatibility complex class II (MHC II) accessory m

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

58 The major histocompatibility complex class II (MHC II)-CD4 immunol

59 lterations in both the CD11c(+) DC and major histocompatibility complex class II (MHC)-II(+) mature a

60 is an immune inhibitory receptor, with major histocompatibility complex class II (MHC-II) as a canoni

61 e-wide CRISPR-Cas9 screening, that the major histocompatibility complex class II (MHC-II) human leuko

62 ides displayed by a defined autoimmune major histocompatibility complex class II (MHC-II) molecule.

63 Major histocompatibility complex class II (MHC-II) molecules o

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

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

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

67 LA-DM) is an integral component of the major histocompatibility complex class II (MHCII) antigen-proc

68 that presentation of such antigens on major histocompatibility complex class II (MHCII) leads to act

69 gens to T cell receptors (TCRs) and/or major histocompatibility complex class II (MHCII) molecules.

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

71 ffector responses during infection was major histocompatibility complex class II (MHCII)-dependent.

72 of the complex of cognate peptide and major histocompatibility complex class II (pMHCII) from the DC

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

74 ntibiotic-induced broad suppression of major histocompatibility complex class II antigen presentation

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

76 deaminase, and immune evasion through major histocompatibility complex class II downregulation, PD-L

77 peripheral T-cell counts, and reduced major histocompatibility complex class II expression levels we

78 s weight, a lymphopenia, a decrease of major histocompatibility complex class II expression on dendri

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

80 D4 T-cell counts and downregulation of major histocompatibility complex class II expression on periph

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

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

86 ded, and the peptides are presented on major histocompatibility complex class II molecules, thereby p

87 bacterial superantigens, which bind to major histocompatibility complex class II on antigen-presentin

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

89 e T-cell-dependent immune responses by major histocompatibility complex class II presentation.

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

91 ecific CD4(+) T-cell populations using major histocompatibility complex class II tetramers in volunte

92 MIA microglia increased expression of major histocompatibility complex class II that was coupled wit

93 the first demonstration that not only major histocompatibility complex class II, but also class I, m

94 The major histocompatibility complex class-I (MHC-I) peptide-loadi

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

96 n 2; myeloperoxidase; lactoperoxidase; major histocompatibility complex, class I, A; major histocompa

97 complex, class II, isotype DR beta I; major histocompatibility complex, class I, C; and major histoc

98 compatibility complex, class I, C; and major histocompatibility complex, class II, isotype DQ beta I.

99 istocompatibility complex, class I, A; major histocompatibility complex, class II, isotype DR beta I;

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

101 hown to be TAAs, their presentation on major histocompatibility complex classes I (MHC-I) and II (MHC

102 leads to long-term (>75 d) survival of major histocompatibility complex-different skin allografts wit

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

104 in solid tumors, HRSCs frequently lack major histocompatibility complex expression, and the mechanism

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

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

107 hly specific and dependent on the host major histocompatibility complex genotype.

108 The major histocompatibility complex haplotype represents the most

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

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

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

112 (ERAP1) and ERAP2 critically shape the major histocompatibility complex I (MHC I) immunopeptidome.

113 macrophages acquire memory specific to major histocompatibility complex I (MHC-I) antigens, and we id

114 ated to epigenetically reverse the low major histocompatibility complex I expression caused by the do

115 T cells owing to the downregulation of major histocompatibility complex I surface expression.

116 d, consequently resulting in increased major histocompatibility complex I surface expression.

117 Major histocompatibility complex II (MHC II) molecules are inv

118 agosomal tubule formation, and impairs major histocompatibility complex II (MHC-II) presentation.

119 h circulating neutrophils, with higher major histocompatibility complex II (MHCII) expression, sugges

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

121 tting H2s or disease-nonpermitting H2b major histocompatibility complex II haplotypes.

122 sclerosis, we used a novel tetramer of major histocompatibility complex II to track T cells reactive

123 ll differentiation, prolonged monocyte major histocompatibility complex II upregulation and persisten

124 These results indicate that major histocompatibility complex II-associated susceptibility

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

126 ciated with expression of genes in the major histocompatibility complex, including C4A and C4B, previ

127 herapies fail to exploit their in situ major histocompatibility complex-independent tumoricidal poten

128 mparable to many alphabeta TCR-peptide major histocompatibility complex interactions.

129 peptides derived from a yeast peptide major histocompatibility complex library of some of the clonal

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

131 To elucidate major histocompatibility complex-linked systemic sclerosis gen

132 geting the BRCA1 gene, the entire 4-Mb major histocompatibility complex locus and 18 well-characteriz

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

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

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

136 Variants in major histocompatibility complex (MHC) and in interferon lambd

137 (TCRs) recognize antigens presented by major histocompatibility complex (MHC) and MHC class I-like mo

138 gens bound to molecules encoded by the major histocompatibility complex (MHC) and presented on the ce

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

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

141 nhibitory NK cell receptors with their major histocompatibility complex (MHC) class I (or HLA class I

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

143 n iPSCs lose their immunogenicity when major histocompatibility complex (MHC) class I and II genes ar

144 l prediction tools to identify LASV GP major histocompatibility complex (MHC) class I and II T-cell e

145 nti-tumor cytolytic activity and lower major histocompatibility complex (MHC) class I gene expression

146 Genetic variability across the three major histocompatibility complex (MHC) class I genes (human le

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

148 ass I (HLA-I) molecules are encoded by major histocompatibility complex (MHC) class I loci in humans.

149 a transcription factor that regulates major histocompatibility complex (MHC) class I molecule expres

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

151 Major Histocompatibility Complex (MHC) class I molecules selec

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

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

154 In SWATH-MS major histocompatibility complex (MHC) class I proteins were h

155 In comparison to the families of major histocompatibility complex (MHC) class I, MHC class II a

156 esented on the cell surface as part of major histocompatibility complex (MHC) class I, suggesting an

157 expressed across primary TCLs, whereas major histocompatibility complex (MHC) class I, which can also

158 Mapping studies with major histocompatibility complex (MHC) class I- and class II-d

159 We identified major histocompatibility complex (MHC) class I-binding epitope

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

161 geting of virus-infected cells and the major histocompatibility complex (MHC) class I-primed CD8(+) T

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

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

164 s by enhancing peptide presentation by major histocompatibility complex (MHC) class I.

165 ein-derived antigens in the context of major histocompatibility complex (MHC) class Ia and class II m

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

167 CD4 T cells and major histocompatibility complex (MHC) class II molecules are

168 s, even in tumours that do not express major histocompatibility complex (MHC) class II molecules.

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

170 n differentiating CD4(+) T cells or of major histocompatibility complex (MHC) class II on intestinal

171 s constitutively express low levels of major histocompatibility complex (MHC) class II proteins, whic

172 hermore find that a variant within the major histocompatibility complex (MHC) class II region contrib

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

174 of chronic typhoid fever combined with major histocompatibility complex (MHC) class II tetramers to i

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

176 n in human cells, we identify that the major histocompatibility complex (MHC) class II transactivator

177 We exemplify this concept with SIEC major histocompatibility complex (MHC) class II, which is diur

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

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

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

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

182 ntigenic peptides displayed in a given major histocompatibility complex (MHC) context.

183 senting cells (APCs) with intact donor major histocompatibility complex (MHC) derived from allograft-

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

185 Major histocompatibility complex (MHC) genes encode proteins t

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

187 atches at half (haploidentical) or all major histocompatibility complex (MHC) genes.

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

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

190 Although allelic diversity at the major histocompatibility complex (MHC) has implications for ad

191 The major histocompatibility complex (MHC) has long served as a mo

192 rally, this approach is referred to as major histocompatibility complex (MHC) homo-to-hetero transpla

193 dence for the role of an allele of the major histocompatibility complex (MHC) I gene HLA-B in the occ

194 tigenic peptides that bind stably to a major histocompatibility complex (MHC) I molecule for display

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

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

197 The major histocompatibility complex (MHC) is a central component

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

199 The major histocompatibility complex (MHC) is responsible for dete

200 The Major Histocompatibility Complex (MHC) is the most genetically

201 est common genetic associations in the major histocompatibility complex (MHC) locus, an association t

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

203 n described in the context of multiple major histocompatibility complex (MHC) mismatches.

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

205 Nonclassical (class-Ib) major histocompatibility complex (MHC) molecules (MHC-Ibs) hav

206 Major histocompatibility complex (MHC) molecules are expressed

207 ngenic mice to examine the function of major histocompatibility complex (MHC) molecules in eliminatio

208 V-7) U21 glycoprotein binds to class I major histocompatibility complex (MHC) molecules in the endopl

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

210 get cells that present cognate peptide-major histocompatibility complex (MHC) molecules.

211 ogenous processing and presentation on major histocompatibility complex (MHC) molecules.

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

213 AnthOligo was tested by capturing the Major Histocompatibility Complex (MHC) of a random sample.The

214 lular form of the TRA and the class of major histocompatibility complex (MHC) on which antigen is pre

215 h the proteins of class I and class II major histocompatibility complex (MHC) pathways.

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

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

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

219 ding strengths to class-I and class-II major histocompatibility complex (MHC) proteins for 284 DNA-ta

220 argeting human leukocyte antigen (HLA)/major histocompatibility complex (MHC) proteins limit successf

221 essed to neo-antigens and presented by major histocompatibility complex (MHC) proteins to T cells.

222 ze short peptide antigens presented on major histocompatibility complex (MHC) proteins.

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

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

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

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

227 Major histocompatibility complex (MHC) restriction is a fundam

228 Major histocompatibility complex (MHC) restriction is a unique

229 n the recovery of haplotype diversity, major histocompatibility complex (MHC) variants, satellite DNA

230 Treg) that recognize the Qa-1 class Ib major histocompatibility complex (MHC), a mouse homolog of hum

231 nocompetence via heterozygosity at the major histocompatibility complex (MHC), a widely-used genetic

232 lular complex comprising a peptide and major histocompatibility complex (MHC), and induce intracellul

233 The interaction between the class I major histocompatibility complex (MHC), the peptide presented

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

235 ested whether genetic variation in the major histocompatibility complex (MHC), which is associated wi

236 We assessed the evidence for major histocompatibility complex (MHC)-based mate preference i

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

238 ee peptides or on those bound to their major histocompatibility complex (MHC)-I-presenting molecules.

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

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

241 HD) largely has been extrapolated from major histocompatibility complex (MHC)-matched murine skin all

242 Using major histocompatibility complex (MHC)-mismatched and MHC-matc

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

244 y the third CDRs (CDR3s) interact with major histocompatibility complex (MHC)-presented epitopes from

245 Major histocompatibility complex (MHC)-related 1-restrictied M

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

247 to human T-cell recognition of murine major histocompatibility complex (MHC).

248 to assemble gene clusters such as the major histocompatibility complex (MHC).

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

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

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

252 ition of antigens presented by class I major histocompatibility complex (MHC-I) proteins on tumor cel

253 uction of recombinant patient-specific major histocompatibility complexes (MHC) loaded with these pep

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

255 tigenic peptides presented by class II major histocompatibility complexes (MHC-II).

256 Retnla, and H2-a/e (encoding class II major histocompatibility complex [MHC] proteins) and many othe

257 ) that present low antigenicity (i.e., major histocompatibility complex, MHC).

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

259 Peptide binding to major histocompatibility complexes (MHCs) is a central compone

260 modeling of peptide display by class I major histocompatibility complexes (MHCs) is essential for pep

261 ed skin transplant model with a single major histocompatibility complex mismatch, we compared the the

262 of Notch-1 receptor inhibition in full major histocompatibility complex-mismatch murine cardiac and l

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

264 Using multimers of peptide major histocompatibility complex molecules (pMHC) and of ICAM-

265 module to recognize peptides bound to major histocompatibility complex molecules (pMHCs) in "vertica

266 he same antigenic peptide presented on major histocompatibility complex molecules but experience disp

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

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

269 t and restricted to the recognition of major histocompatibility complex molecules presenting peptide

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

271 ked SNPs in distinct blocks within the major histocompatibility complex on 6p21.

272 regulation of class I molecules of the major histocompatibility complex on tumour cells.

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

274 ical tolerance by down-regulating both major histocompatibility complex pathways (MHC I and II).

275 fundamental metric of diversity at the major histocompatibility complex-peptide complex, which dictat

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

277 The natural peptide-major histocompatibility complex (pMHC) ligand for T cell rece

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

279 eptor (TCR) binding to agonist peptide major histocompatibility complex (pMHC) triggers signaling eve

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

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

282 esented as processed peptides bound to major histocompatibility complexes (pMHC).

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

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

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

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

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

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

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

290 t peptides are presented to the TCR by major histocompatibility complex proteins expressed by antigen

291 by trimming peptides for loading onto major histocompatibility complex proteins.

292 ell and solid-organ transplantation, and the histocompatibility complex region exhibits countless gen

293 ignaling, psoriasis pathology, and the major histocompatibility complex region.

294 o perform detailed fine-mapping of the major-histocompatibility-complex region, we conducted next-gen

295 antigens presented on non-polymorphic major histocompatibility complex-related 1 (MR1) molecules.

296 nic SIV challenge virus, non-canonical major histocompatibility complex restriction, and absent antib

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

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

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

300 er, three in the Dunedin study) in the major histocompatibility complex, which were associated with e