ライフサイエンスコーパス: histocompatibility

1 We disrupted the histocompatibility 2, class II antigen A, beta 1 gene (H

2 his was demonstrated by the observation that histocompatibility 2, Q region locus 10 (H2-Q10) is a hi

3 w Transplant Research, jointly with the NMDP Histocompatibility Advisory Group, provide evidence-base

4 -/-) ), we show that the transplant of minor histocompatibility Ag (HY)-mismatched skin grafts from T

5 ein TS1 CD4 cells specific for a model minor histocompatibility Ag (miHA) induce GVHD in miHA-positiv

6 e annual meeting of the American Society for Histocompatibility and Immunogenetics in Pittsburgh, PA

7 y of Transplantation and American Society of Histocompatibility and Immunogenetics membership.

8 ed down for non-"quality" reasons, primarily histocompatibility and size.

9 ed major HLA disparities or expressing minor histocompatibility antigen (miHA) differences presented

10 Minor histocompatibility antigen (MiHA)-specific T cells were

11 peptide peptidase (SPP), also known as minor histocompatibility antigen H13.

12 mediated by T cells that recognize the minor histocompatibility antigen H60.

13 RHGDIB) (adjusted MFI [aMFI]>=1000), a minor histocompatibility antigen, associated with graft failur

14 orescence intensity [aMFI] >= 1000), a minor histocompatibility antigen, associated with graft failur

15 compatibility complex-matched multiple minor histocompatibility antigen-mismatched alloHCT using bone

16 In both a minor histocompatibility antigen-mismatched as well as a MHC-h

17 t the LIMS1 locus appeared to encode a minor histocompatibility antigen.

18 ing tumor-specific antigens (TSAs) and minor histocompatibility antigens (MiHAs).

19 vances in systematic identification of minor histocompatibility antigens and neoantigens arising from

20 ances pathogenicity by down-regulating major histocompatibility class I (MHC-I) expression to evade k

21 me that optimizes the peptide cargo of major histocompatibility class I (MHC-I) molecules and regulat

22 miallogeneic donor cells mismatched at major histocompatibility class I can enhance tolerance to subs

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

24 odel induced by a single DST across an major histocompatibility class I mismatch in an unmanipulated

25 evels of two different substrates: the major histocompatibility class I molecule HLA-A2 and the T-cel

26 ell priming required the expression of major histocompatibility class I molecules by cDC1.

27 In patients, expression of major histocompatibility class II in melanoma is linked to fav

28 Ags), which engage lateral surfaces of major histocompatibility class II molecules and T-cell recepto

29 sing by cDC2, as selective deletion of major histocompatibility class II molecules in cDC1 also preve

30 Furthermore, deletion of either major histocompatibility class II or CD40 in cDC1 impaired tum

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

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

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

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

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

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

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

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

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

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

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

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

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

44 Major Histocompatibility Complex (MHC) class I molecules selec

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

75 Major histocompatibility complex (MHC) genes encode proteins t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 Major histocompatibility complex (MHC) molecules are expressed

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

217 The major histocompatibility complex haplotype represents the most

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

263 1 subunit of adaptor protein 1 and the major histocompatibility complex-1 tail, and subsequent major

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

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

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

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

268 To elucidate major histocompatibility complex-linked systemic sclerosis gen

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

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

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

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

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

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

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

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

277 rget peptide antigens presented by the major histocompatibility complex.

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

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

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

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

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

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

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

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

286 donor T cells specific for particular minor histocompatibility (H) antigens.

287 olecular mismatch analysis for assessment of histocompatibility in transplantation requires high-reso

288 years ago, we reported the first successful histocompatibility leukocyte antigen-matched sibling don

289 rated the feasibility of performing combined histocompatibility leukocyte antigen-matched, sibling do

290 of African ancestry enrichment at the major histocompatibility locus on chromosome 6, consistent wit

291 tity bound to both dendritic cell (DC) major histocompatibility (MHC) class I and MHC class II--stron

292 endent on CD103(+) dendritic cells and major histocompatibility (MHC) class Ia molecules.

293 We found that human and minor histocompatibility-mismatched donor mouse heart allograf

294 We have reported that the major histocompatibility molecule HLA-DQ2 (DQA1*05:01/DQB1*02:

295 , we employ synTacs, which are dimeric major histocompatibility molecule scaffolds of defined composi

296 tem's ability to recognize peptides on major histocompatibility molecules contributes to the eradicat

297 antibodies-increases the expression of major histocompatibility protein class I (MHC I) proteins on t

298 table patterns, which can be identified with histocompatibility strategies, and SLA class I is a poss

299 rnosa defects in a rabbit model to show good histocompatibility with no immunological rejection, supp

300 ributed by participants of the International Histocompatibility Working Group in Hematopoietic Cell T