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

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

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

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

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

5 even when the tumour and host share the same major histocompatibility complex alleles, the most poten

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

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

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

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

10 rong signals of selection at lactase and the major histocompatibility complex, and in favor of blond

11 pes at numerous sites, often on incompatible major histocompatibility complex, and occurs in the cont

12 sic three-way interaction among antigen, the major histocompatibility complex, and the T cell recepto

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

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

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

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

17 fy beta2-microglobulin (B2M), a component of major histocompatibility complex class 1 (MHC I) molecul

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

19 6 was markedly more effective at suppressing major histocompatibility complex class I (MHC I) display

20 our cells depends on antigen presentation by major histocompatibility complex class I (MHC I) molecul

21 Major histocompatibility complex class I (MHC I) positiv

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

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

24 0I, unexpectedly and uniquely degraded Nef's major histocompatibility complex class I (MHC-I) downreg

25 LCMV V35A) bearing a mutation in the cognate major histocompatibility complex class I (MHC-I) epitope

26 Flow cytometry analyses showed decreased major histocompatibility complex class I (MHC-I) express

27 inactivating mutations that lead to loss of major histocompatibility complex class I (MHC-I) express

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

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

30 ins that modulate cell surface expression of major histocompatibility complex class I (MHC-I) molecul

31 inst NS5 were also elicited, as evidenced by major histocompatibility complex class I (MHC-I) tetrame

32 nt molecules involved in these events is the Major Histocompatibility Complex class I (MHC-I), respon

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

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

35 n subjects with ALS reduce the expression of major histocompatibility complex class I (MHCI) molecule

36 Major histocompatibility complex class I (MHCI) proteins

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

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

39 blood mononuclear cell DEGs associated with major histocompatibility complex class I and natural kil

40 er-cell immunoglobulin-like receptors (KIR), major histocompatibility complex class I chain-related g

41 erefore, the identification of antigens with major histocompatibility complex class I epitopes is a c

42 Major histocompatibility complex class I expression on M

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

44 ike receptor (iKIR) for which the respective major histocompatibility complex class I ligand is absen

45 usly generating peptides that could serve as major histocompatibility complex class I ligands, markin

46 Major histocompatibility complex class I molecules (MHC

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

48 mor growth of melanoma cell lines expressing major histocompatibility complex class I molecules at hi

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

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

51 Major histocompatibility complex class I polypeptide-rel

52 esponsiveness requires positive selection on major histocompatibility complex class I-associated pept

53 on of bacterial metabolites presented by the major histocompatibility complex class I-related molecul

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

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

56 en, characterized by increased expression of major histocompatibility complex class II (approximately

57 e developed a mouse strain that lacks murine major histocompatibility complex class II (MHC II) and i

58 Inoculation with M. canis also decreased major histocompatibility complex class II (MHC-II) antig

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

60 r (CIITA) is essential for the expression of major histocompatibility complex class II (MHC-II) genes

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

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

63 en presentation in addition to the classical major histocompatibility complex class II (MHC-II) pepti

64 ific for mouse CMV (MCMV) epitopes and use a major histocompatibility complex class II (MHC-II) tetra

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

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

67 A polymorphism at beta57 in some major histocompatibility complex class II (MHCII) allele

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

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

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

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

72 utoimmune-disease-relevant peptides bound to major histocompatibility complex class II (pMHCII) molec

73 gin when naive CD4(+) T cells engage peptide+major histocompatibility complex class II and co-stimula

74 ent with AZD1480 inhibited alpha-SYN-induced major histocompatibility complex Class II and inflammato

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

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

77 ed 44 epitopes that are predicted to be good major histocompatibility complex class II binders and at

78 Major histocompatibility complex class II binding and T-

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

80 or X, two transcription factors dedicated to major histocompatibility complex class II expression, su

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

82 We used major histocompatibility complex class II mismatched C57

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

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

85 enabled the presentation of self antigens by major histocompatibility complex class II molecules in a

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

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

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

89 Furthermore, silencing of major histocompatibility complex class II reduces alloge

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

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

92 rturbed 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+ im

94 Major histocompatibility complex class II, a marker of m

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

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

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

98 ssed LMO2, CD58, and stromal-1-signature and major histocompatibility complex class II-signature gene

99 469 located on 6p22.1, and covering lncRNAs (major histocompatibility complex, class I, A (HLA-A) and

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

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

102 veral classically used exosome markers, like major histocompatibility complex, flotillin, and heat-sh

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

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

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

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

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

108 ctively present survivin peptides on class I major histocompatibility complex, had significantly dimi

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

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

111 Those results revealed two major histocompatibility complex haplotypes associated w

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

113 ficient mice, patient cells showed increased major histocompatibility complex I expression and most C

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

115 pes, the peptides that bind to non-classical major histocompatibility complex Ib Qa-1 molecules and a

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

117 polyclonal stimulation, and displayed lower major histocompatibility complex II expression by antige

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

119 Major histocompatibility complex II tetramers correspond

120 an increased number of microglia expressing major histocompatibility complex II.

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

122 r directly or related to the function of the Major Histocompatibility Complex in a number of differen

123 we investigate the plasticity of a class II major histocompatibility complex in the absence of a bou

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

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

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

127 To elucidate major histocompatibility complex-linked systemic scleros

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

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

130 ger leukocytes (but not the parenchyma) were major histocompatibility complex-matched to the recipien

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

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

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

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

135 The skin constructs were transplanted across major histocompatibility complex (MHC) barriers in a por

136 ll (DC) maturation, as well as inhibition of major histocompatibility complex (MHC) class I and class

137 at BDLF3 downregulates expression of surface major histocompatibility complex (MHC) class I and class

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

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

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

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

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

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

144 Major histocompatibility complex (MHC) class I molecules

145 silico methods predicting peptide binding to major histocompatibility complex (MHC) class I molecules

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

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

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

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

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

151 f G-protein signaling, and downregulation of major histocompatibility complex (MHC) class I surface e

152 :01-positive patients analyzed by performing major histocompatibility complex (MHC) class I tetramer

153 ed cells is characteristically restricted by major histocompatibility complex (MHC) class I, although

154 killer cells express multiple receptors for major histocompatibility complex (MHC) class I, includin

155 c acid early inducible-1 (Rae-1) in mice and major histocompatibility complex (MHC) class I-chain-rel

156 Rs recognize lipid antigens presented by the major histocompatibility complex (MHC) class I-like mole

157 ds (NKG2DLs) are a group of stress-inducible major histocompatibility complex (MHC) class I-like mole

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

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

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

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

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

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

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

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

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

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

168 distinguished CD4(+) T cells selected by the major histocompatibility complex (MHC) class II molecule

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

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

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

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

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

174 ted lymphocytes to be targeted by a panel of major histocompatibility complex (MHC) class II-matched

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

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

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

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

179 The major histocompatibility complex (MHC) contains the most

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

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

182 Previous studies have indicated that the major histocompatibility complex (MHC) genes play the mo

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

184 t retain immunogenicity depends on both host major histocompatibility complex (MHC) genetics and the

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

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

187 The chicken major histocompatibility complex (MHC) has strong geneti

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

189 can operate simultaneously by analysing the major histocompatibility complex (MHC) in guppies (Poeci

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

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

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

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

194 1 at microsatellite, structural variant, and major histocompatibility complex (MHC) loci, confirming

195 The Major Histocompatibility Complex (MHC) locus encodes cla

196 a population level involves variation in the major histocompatibility complex (MHC) locus, but the ge

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

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

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

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

201 6 haplotype encoding the HLA-C*08:02 class I major histocompatibility complex (MHC) molecule.

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

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

204 n of protein antigens on the cell surface by major histocompatibility complex (MHC) molecules coordin

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

206 alphabeta T cell receptor (TCR) with peptide-major histocompatibility complex (MHC) molecules on anti

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

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

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

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

211 Major Histocompatibility Complex (MHC) or Human Leukocyt

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

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

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

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

216 gth with which complexes of self peptide and major histocompatibility complex (MHC) proteins are reco

217 T cells reactive to complexes of peptide and major histocompatibility complex (MHC) proteins, many ot

218 d variants expanding throughout the extended major histocompatibility complex (MHC) region and 68 non

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

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

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

222 41270488) for HPV8 seropositivity within the major histocompatibility complex (MHC) region.

223 oci, with the strongest association from the major histocompatibility complex (MHC) region.

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

225 Major histocompatibility complex (MHC) restriction is a

226 Major histocompatibility complex (MHC) restriction is a

227 variant mapping, independent localization of major histocompatibility complex (MHC) risk from classic

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

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

230 , including the tumor necrosis factor (TNF), major histocompatibility complex (MHC), interleukin 23 r

231 nt, have been implicated in vertebrates: the major histocompatibility complex (MHC), which could be v

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

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

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

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

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

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

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

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

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

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

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

246 g B-cell selection by sensing the density of major histocompatibility complex (MHC):peptide antigen c

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

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

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

250 ixed-chimerism model receiving BCNU across a major histocompatibility complex mismatch.

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

252 We performed major histocompatibility complex mismatched aorta to car

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

254 topic transplants were performed using minor major histocompatibility complex-mismatched B6.C-H2 dono

255 Using the major histocompatibility complex-mismatched mouse orthot

256 parenchyma and the passenger leukocytes were major histocompatibility complex-mismatched to the recip

257 rk Agouti rat and Balb mouse donors to fully major histocompatibility complex-mismatched Wistar Furth

258 in kidney allograft rejection using a fully major histocompatibility complex-mismatched, life-sustai

259 R engages a peptide bound to the restricting major histocompatibility complex molecule (pMHC), it tra

260 lf and foreign peptide antigens presented in major histocompatibility complex molecules (pMHC) is ess

261 ntigenic peptides within class I or class II major histocompatibility complex molecules (pMHCI or pMH

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

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

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

265 s (TCRs) recognize agonist peptides bound to major histocompatibility complex molecules on antigen-pr

266 of T cell responses is complex and involves major histocompatibility complex molecules on transplant

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

268 ce of interleukin-21 and enriched by peptide-major histocompatibility complex multimer-guided cell so

269 specific CD8 T cells were tracked down using major histocompatibility complex multimers against the i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

287 ct with foreign antigens bound to alleles of major histocompatibility complex proteins (MHC) that the

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

289 n signals for oligoclonal band status in the major histocompatibility complex region for the rs927164

290 Association within the major histocompatibility complex region was also observe

291 We identify two novel associations in the major histocompatibility complex region with immunoglobu

292 161(+) MAIT cells, surface expression of the major histocompatibility complex-related protein 1 (MR1)

293 enabling antigen recognition independent of major histocompatibility complex restriction, while reta

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

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

296 a fundamental difference between the CD1 and major histocompatibility complex systems is that all hum

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

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

299 nsity single nucleotide polymorphisms of the major histocompatibility complex to precisely identify r

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