ライフサイエンスコーパス: MHC

1 MHC class I transactivator (CITA), NLRC5 [nucleotide-bin

2 MHC class I-related molecule MR1 presents riboflavin- an

3 MHC class I-restricted spliced epitopes have been descri

4 MHC I molecules possess an intrinsic ability to discrimi

5 MHC I molecules typically bind peptides with 9 amino aci

6 MHC-E is a highly conserved nonclassical MHC class Ib mo

7 MHC-I molecules expose the intracellular protein content

8 For 95 MHC homozygous cell lines we assembled, de novo, a set o

9 ompatibility antigen-mismatched as well as a MHC-haploidentical model of sclerodermatous cGVHD, pirfe

10 te major histocompatibility complex class A (MHC-A) and MHC-B from the cell surface.

11 proteins differed markedly in their absolute MHC-A and MHC-B downregulation abilities, all lentiviral

12 In addition, acquired MHC-class I:peptide complexes stimulate T cell responses

13 +) mice: T cells recognizing intact acquired MHC alloantigens proliferated, whereas those responding

14 , we focused on the contribution of acquired MHC-class I on recipient DCs during the life span of a s

15 RPalpha(+)) and CD8alpha(+) readily acquired MHC class I and II from thymic epithelial cells but plas

16 or-cell specific; thymic DC readily acquired MHC from TEC plus thymic or splenic DC, whereas thymic o

17 ility at neutral microsatellite and adaptive MHC genetic variation over five decades in four marginal

18 ic microenvironments generates both adaptive MHC restricted alphabetaT-cells and innate CD1d-restrict

19 n (IL)-2, but not IL-17A; iii) high-affinity MHC class II interaction with SAgs, but not MHC-related

20 n associated with an immune response against MHC-mismatched grafted cells.

21 cognized antigenic peptides presented by all MHC-E molecules tested, including cross-species recognit

22 ependent on features unique to both the allo-MHC and the NS3 epitope.

23 Included are six alternative MHC reference sequences of the human genome that we comp

24 leukemias, we determined that BC-CML and AML MHC upregulation required IFN-gamma stimulation, whereas

25 Unlike effector CD4(+) T cells, an MHC class II tetramer reagent specific for T. gondii did

26 ents-CCAAT, TATAA-like, Sp1BS, and Inr-of an MHC class I gene in primary B-cells during both basal an

27 Here we show an MHC-I-dependent correlation between DNAM-1 expression an

28 NKT cell-activating glycolipid linked to an MHC class I-restricted peptide from a viral antigen in h

29 f an adoptive CD4(+) T-cell therapy using an MHC class II-restricted, HLA-DPB1*0401-restricted TCR th

30 iffered markedly in their absolute MHC-A and MHC-B downregulation abilities, all lentiviral Nef linea

31 stocompatibility complex class A (MHC-A) and MHC-B from the cell surface.

32 gulation of costimulatory molecules CD86 and MHC class II on moDCs induced by B cells.

33 y a dramatic upregulation of CD83, CD86, and MHC class I in response to TLR3 and TLR7/8-agonists.

34 tion markers, that is, CD40, CD80, CD86, and MHC class II molecules.

35 However, the precise mechanism of CIITA and MHC-II down-regulation is not well studied.

36 estingly, the expression levels of CIITA and MHC-II significantly increased when CML stem/progenitor

37 ssion of class-II transactivator (CIITA) and MHC-II expression in infected macrophages.

38 enza- and 3 allergen-derived MHC class I and MHC class II candidate T-cell epitopes with potential an

39 formation on how TCRs engage with MHC-Ia and MHC-II, our understanding of TCR/MHC-Ib interactions is

40 rences in infection status, cell lineage and MHC class II expression by antigen-bearing cells correla

41 reactivity can proceed with high peptide and MHC specificity.

42 ms that influence how TCRs bind peptides and MHC proteins.

43 ect evidence for coevolution between TCR and MHC genes, helping to explain how MHC compatibility and

44 This process is sensitive to anti-MHC class II antibodies.

45 a manner similar to that observed with anti-MHC class II.

46 TLA-4 interaction with CD80/CD86, as well as MHC class II-TCR interaction within mouse Treg pools and

47 sponses and the epitope preferentially binds MHC class II/IA(k) rather than IE(k) By creating IA(k)/a

48 s progressively downregulated following both MHC and CD1d-restricted thymic selection events.

49 Activation of T helper cells by MHC-II on Schwann cells thus promotes post-traumatic axo

50 ell-associated Ags into peptide displayed by MHC I is however defective in hepatocytes lacking collec

51 ength of a TCR for self-peptide presented by MHC (self-pMHC) impacts T cell function, we sought to de

52 ed on recognizing oligopeptides presented by MHC class I molecules.

53 cascades upon binding antigens presented by MHC-family proteins on antigen-presenting cells.

54 hanistically, CDR3 networks were promoted by MHC-mediated selection, and were reduced following immun

55 l responses that were entirely restricted by MHC II or the nonclassical MHC I molecule, MHC-E.

56 that is disconnected from TCR restriction by MHC.

57 to peptides presented on the cell surface by MHC class I molecules.

58 (-) cDC, expressing higher levels of CD172a, MHC class II and CD11b.

59 alters the quantity of production of certain MHC I epitopes but does not appear to be preferentially

60 To investigate myosin heavy chain (MHC) phosphorylation roles in 3D migration, we expressed

61 without salt (Lot A), no myosin heavy chain (MHC) polymerization was observed, only aggregation, as i

62 this approach to systematically characterize MHC ligands from 17 patients.

63 responsible for the down-regulation of CIITA/MHC-II by inducing H3K9me2/3.

64 ction down-regulated the expression of CIITA/MHC-II by inducing hypermethylation in histone H3 lysine

65 mmon major histocompatibility complex class (MHC-II) epitope was identified, based on in silico predi

66 , included cells restricted by non-classical MHC molecules and expressed the receptor NK1.1, the inte

67 ng antibodies independently of the classical MHC haplotype.

68 were identified as conventional classically MHC I restricted, and we found no evidence for MHC II or

69 quired IFN-gamma stimulation, whereas CP-CML MHC upregulation was independent of both the IFN-gamma r

70 trate that an integrative approach combining MHC isolation, peptide identification, and exome sequenc

71 ion by the major histocompatibility complex (MHC) and subsequent recognition by T cells.

72 esented by major histocompatibility complex (MHC) class I and class II molecules.

73 l role for major histocompatibility complex (MHC) class I in controlling the phagocytic function of m

74 esented on major histocompatibility complex (MHC) class I molecules in an autophagy-dependent fashion

75 surface by major histocompatibility complex (MHC) class I molecules.

76 ntation by major histocompatibility complex (MHC) class I proteins initiates CD8(+) T cell-mediated i

77 ted by the major histocompatibility complex (MHC) class I-related molecule MR1.

78 hat encode major histocompatibility complex (MHC) class I-restricted T-cell receptors (TCRs) or chime

79 predicted major histocompatibility complex (MHC) class II binding peptides.

80 ading onto major histocompatibility complex (MHC) class II molecules.

81 Recently, major histocompatibility complex (MHC) class II tetramers have emerged as a powerful tool

82 coding the major histocompatibility complex (MHC) class II transactivator, CIITA.

83 generated major histocompatibility complex (MHC) class II-restricted T cell hybridomas from IKEPLUS-

84 The major histocompatibility complex (MHC) contains the most polymorphic genetic system in hum

85 The Major Histocompatibility Complex (MHC) is a key component of the adaptive immune system of

86 al setting.Major histocompatibility complex (MHC) matching improves graft survival rates after organ

87 on exposed major histocompatibility complex (MHC) polymorphisms or the degenerate recognition of allo

88 nclassical major histocompatibility complex (MHC) protein CD1d, which presents lipid antigens to iNKT

89 ted by the major histocompatibility complex (MHC) protein which is encoded by the human leukocyte ant

90 mammalian Major Histocompatibility Complex (MHC) region contains several gene families characterized

91 within the major histocompatibility complex (MHC) region were observed to be strongly associated with

92 ll surface major histocompatibility complex (MHC)-I molecule expression.

93 show that major histocompatibility complex (MHC)-II and its master regulator class II transactivator

94 including major histocompatibility complex (MHC)-restricted alphabeta T cell receptor (TCR) T cells

95 he TCR and major histocompatibility complex (MHC).

96 Consequently, MHC-matching increases the survival of grafted dopamine

97 opes in clade C virus infection, constructed MHC class II tetramers, and then used these to define th

98 t lactational transfer of immunity can cross MHC class I barriers and that Th1 immunity can be impart

99 oss-presentation to autoaggressive cytotoxic MHC-E-restricted CD8(+)CD56(+) T cells.

100 Nlrc5(-/-) mice have decreased MHC-I expression on hematopoietic cells and fewer CD8(+)

101 matic mutations is associated with defective MHC class I expression, impaired cytotoxic T cell activa

102 entified 4 influenza- and 3 allergen-derived MHC class I and MHC class II candidate T-cell epitopes w

103 that Nef's inferior ability to downregulate MHC-B compared to that of MHC-A is conserved across prim

104 s, all lentiviral Nef lineages downregulated MHC-A, on average, 11 to 32% more efficiently than MHC-B

105 le to handle the varied requirements of each MHC-group.

106 Disruption of either MHC class I or LILRB1 potentiated phagocytosis of tumor

107 that carriage of Nef variants with enhanced MHC-B downregulation ability is associated with reduced

108 ong linkage disequilibrium across the entire MHC complex.

109 Fast-evolving MHC class I polymorphism serves to diversify NK cell and

110 Two hypotheses have been proposed to explain MHC specificity of T cells.

111 Natural killer (NK) cells express MHC class I (MHC-I)-specific receptors, such as Ly49A, t

112 sed of approximately 67% fast-twitch fibers (MHC IIa+IId).

113 idence for the germline encoded TCR bias for MHC, and for the coreceptor sequestration model in the c

114 loads than residents, after controlling for MHC genotype rarity.

115 C I restricted, and we found no evidence for MHC II or HLA-E restriction.

116 rol NK-cell activation and are necessary for MHC-I-dependent education, we investigated whether DNAM-

117 Our results demonstrate the rationale for MHC-matching in neural cell grafting to the brain and it

118 ed from endogenous and exogenous sources for MHC class I and class II molecules, respectively.

119 ons with Ag receptors specific for a foreign MHC class II molecule type loaded with peptides from leu

120 l divisions from C57BL/6 donors but not from MHC class II- or CD40-deficient donors.

121 mote long-term allograft allografts in fully MHC-disparate strains.

122 ed peripheral blood HSCT in unrelated, fully MHC-matched Mauritian-origin cynomolgus macaques.

123 of NMIIA or cells expressing the mutant GFP MHC-IIA display severe defects in invasion and in stabil

124 ollagen gels, cells expressing wild-type GFP MHC-IIA behave like parental cells, displaying robust an

125 methylated regions on chromosome 6 harboring MHC gene clusters.

126 rst long-read sequence assembly of the horse MHC class II region with rigorous manual gene annotation

127 t a reliable reference sequence of the horse MHC region.

128 to Ag-loaded exosomes were dependent on host MHC class I, with a critical role for splenic langerin(+

129 en TCR and MHC genes, helping to explain how MHC compatibility and bias can be encoded within TCRs.

130 Due to this complexity, however, MHC remains to be characterized in many species includin

131 Human MHC II yielded greater thymic output and a more diverse

132 cells selected from a single mouse or human MHC class II (MHC II) in mice containing the human TCR g

133 8(+) T cell response restricted by the human MHC-Ib molecule human leukocyte antigen (HLA)-E and spec

134 of the full extracellular domain of class I MHC molecules such as H-K(b), we produced a truncated fo

135 s recognize lipid Ags presented by a class I MHC-like molecule CD1d, a member of the CD1 family.

136 internalization and subsequent MHC class I (MHC I) display of extracellular Ags.

137 es major histocompatibility complex class I (MHC-I) expression during various types of infections, bu

138 tural killer (NK) cells express MHC class I (MHC-I)-specific receptors, such as Ly49A, that inhibit k

139 nt mice, and treatment with an anti-class II MHC antibody abrogated its antitumor activity.

140 important contribution of a single class II MHC-peptide complex to the immune response against HIV-1

141 d from a single mouse or human MHC class II (MHC II) in mice containing the human TCR gene loci.

142 l major histocompatibility complex class II (MHC-II)-like molecule H2-O, a negative regulator of anti

143 a major histocompatibility complex class II (MHC-II; HLA-DR)-dependent manner.

144 epithelial cell (mTEC) lineage from immature MHC class II (MHCII)(lo) to mature MHCII(hi) mTECs has r

145 geting cancer cells with intact and impaired MHC class I-related APM.

146 l analyses suggested that the association in MHC is stronger in samples from North America than those

147 that maintain high linkage disequilibrium in MHC haplotype blocks.

148 between DNAM-1 and NKG2A that occurs even in MHC class I deficient mice.

149 found that the 33-kb Ltab-Ncr3 haplotype in MHC-III was linked to the induction of arthritis with in

150 he quantitative cause-effect relationship in MHC-II-dependent normal and autoimmune responses.

151 ulsed MoDC, the duration of KLH residence in MHC class II loading compartments was significantly redu

152 mediators of antigen presentation, including MHC class I and beta2 microglobulin, were highly suscept

153 eadily internalized by B cells and increased MHC-II expression on monocytes compared with EVs from yo

154 les, we show that positive selection-induced MHC bias of T cell receptors is affected both by the ger

155 ivated CD4 and CD8 genes in mice with intact MHC class I and class II molecules with the hypothesis t

156 Intercellular MHC transfer was donor-cell specific; thymic DC readily

157 ly regulates processing of engulfed Ags into MHC I:peptide complexes within hepatocytes.

158 We investigated MHC-II-mediated protection from type 1 diabetes using a

159 e first release of the database in 2003, IPD-MHC has grown and currently hosts a number of specific s

160 escribe the latest database release, the IPD-MHC 2.0 and discuss planned developments.

161 The IPD-MHC Database project collects and expertly curates seque

162 initiates upon the binding of peptide-loaded MHC (pMHC) on an antigen-presenting cell to the T cell r

163 its T cell receptor (TCR) for peptide-loaded MHCs (pMHC) on an antigen-presenting cell.

164 Here the authors show that in macaques, MHC-matched iPSC-derived neurons provide better engraftm

165 cifically captures and sequences the 4.8-Mbp MHC region from genomic DNA.

166 fector subsets, including ThCTL that mediate MHC class II-restricted cytotoxicity.

167 cetylcholine receptor (AChR) response in MG, MHC class II and alpha-AChR subunit as well as chemokine

168 y MHC II or the nonclassical MHC I molecule, MHC-E.

169 istocompatibility complex class I molecules (MHC I) help protect jawed vertebrates by binding and pre

170 we provide new insights into how monomorphic MHC molecules interact with T cells.

171 t superantigens more efficiently than murine MHC class II molecules, CD4 CD8 double knockout (DKO) mi

172 tion of hundreds of peptides bound to murine MHC class II (MHCII) molecules.

173 This study hence defines MICA as a new, MHC-linked, yet HLA-independent, pSS risk locus and open

174 We discovered a non-MHC-linked Ir gene in a T cell receptor (TCR) locus that

175 habeta T cell receptor (TCR) T cells and non-MHC-restricted gammadelta TCR T cells.

176 MHC-E is a highly conserved nonclassical MHC class Ib molecule that predominantly binds and prese

177 ely restricted by MHC II or the nonclassical MHC I molecule, MHC-E.

178 MHC class II interaction with SAgs, but not MHC-related protein 1 (MR1) participation, is required f

179 eded for the regulatory T cell (Treg) arm of MHC class II responses.

180 supports both helper and regulatory arms of MHC class II responses.

181 Phylogenetic analysis identified a clade of MHC-B, defined by residues 45-74 of the alpha1 domain, w

182 ng 5], is a key transcription coactivator of MHC class I genes.

183 croglobulin (B2M), an essential component of MHC class I antigen presentation, in 29.4% of patients w

184 We demonstrate that deletion of MHC-II in myelinating Schwann cells reduces thermal hype

185 These defects in the expression of MHC class II and costimulatory molecules corresponded wi

186 c forms and cysts, reduced the expression of MHC class II and the costimulatory molecule CD40 on the

187 cell development, precedes the expression of MHC-I-specific inhibitory receptors, and is modulated in

188 observed significantly higher frequencies of MHC class II tetramer-positive CD4(+) T cells in HIV con

189 Sub-functionalisation of MHC alleles into 'supertypes' explains how polymorphisms

190 D8 coreceptors is critical for generation of MHC specificity.

191 Here, we characterized the genes of MHC class IIB chain of the Midas cichlid species complex

192 populations responding weakly to hundreds of MHC-bound peptides from graft-derived leukocytes.

193 ws combinatorial fine-tuning of the level of MHC class I gene expression in response to intrinsic and

194 hibiting EMT markers expressed low levels of MHC-I, high levels of PD-L1, and contained within their

195 arcinoma cell lines expressed high levels of MHC-I, low levels of PD-L1, and contained within their s

196 Loss of MHC class I has been described as a major immune evasion

197 ciated with reduced breadth and magnitude of MHC-B-restricted cellular immune responses in HIV-infect

198 he diverse TCRs interact with a multitude of MHC molecules is unresolved.

199 ns and MCM, RM expressed a greater number of MHC-E alleles at both the population and individual leve

200 With the use of a panel of MHC-III recombinant inbred strains, we found that the 33

201 of CD4(+) T cells and a large population of MHC class II-restricted CD8alphaalpha T cells that are g

202 ll specificity depends on the recognition of MHC class I-epitope complexes at the cell surface.

203 led to rescue Nef-induced down-regulation of MHC class I, suggesting a possible mechanism for attacki

204 tional APCs, but the functional relevance of MHC-II expression by Schwann cells has not been studied

205 d has one of the most diverse repertoires of MHC class IIB genes known, which could serve as a powerf

206 ucture captures a peptide-receptive state of MHC I and provides insights into the mechanism of peptid

207 We report the crystal structure of MHC I in complex with the peptide editor TAPBPR (TAP-bin

208 show that the exposed recognition surface of MHC-bound peptides accessible to the TCR contains suffic

209 in (CD74) mediates assembly and targeting of MHC class II (MHCII) complexes.

210 ocessing (NLP) domain to address the task of MHC-peptide binding prediction.

211 ty to downregulate MHC-B compared to that of MHC-A is conserved across primate lentiviruses and sugge

212 To address their relative dependence on MHC-II, we established a novel ENU-induced mutant mouse

213 iated loading of high-affinity peptides onto MHC I is a key step in the MHC I antigen presentation pa

214 extensive and unexpected diversity in other MHC genes; an example is MUC22, which encodes a lung muc

215 lesions, recognized distinct non-overlapping MHC-class-II-restricted peptides derived from the same p

216 -major histocompatibility complex class I (p-MHC I) proteins displayed by antigen-presenting cells.

217 e-loaded major histocompatibility complex (p/MHC) leads to T-cell activation is not yet fully underst

218 ural changes that accompany binding to its p/MHC ligand (P18-I10/H2-D(d)).

219 ion from autoimmunity afforded by particular MHC/HLA alleles can operate via intestinal microbes, hig

220 We found that patient MHC-I genotype-based scores could predict which mutation

221 (TCR) exhibit high affinity to self-peptide MHC complexes (self pMHC) to avoid autoimmune diseases,

222 f conserved binding topology for TCR-peptide MHC complexes.

223 ese results suggest that Ag dose and peptide-MHC complex stability can lead to multiple fates of insu

224 itro to varying densities of cognate peptide-MHC ligand followed by ligand-free culture in IL-2, we f

225 between the TCR heterodimer and its peptide-MHC ligand derives largely from the juxtaposed hypervari

226 her energy conformations than native peptide-MHC complexes.

227 In the past, predictors of peptide-MHC interactions have primarily been trained on binding

228 ajor histocompatibility complex (TCR-peptide-MHC) reactivity can contribute to the potent antiviral c

229 guished by crossing angles of TCR to peptide-MHC of 29 degrees for F50 versus 69 degrees for JM22 and

230 data on heterotropic allostery where peptide-MHC and membrane cholesterol serve opposing functions as

231 a significant distance from the TCR.peptide.MHC-binding site, remarkably affected ligand binding.

232 onses as they specifically recognize peptide/MHC complexes with their T-cell receptors and initiate a

233 eceptor (TCR) interactions with self-peptide/MHC, whereas unconventional alphabeta T cells, such as T

234 ne-capture assays, and staining with peptide:MHC class II multimers, all of these have significant te

235 nd conditions, in which we show that peptide:MHCs and anti-CD3 antibodies trigger a fraction of T cel

236 umber of peptides complement the polymorphic MHC specificity determining pockets in a way that leads

237 lecule that predominantly binds and presents MHC class Ia leader sequence-derived peptides for NK cel

238 owever, the instability of peptide-receptive MHC molecules has hindered characterization of such conf

239 the addition of peptide to peptide-receptive MHC molecules.

240 Furthermore, blocking PI3K signaling reduced MHC acquisition by thymic CD8alpha(+) cDC and plasmacyto

241 d a substantial database of robust reference MHC haplotype sequences that will enable future populati

242 estimate these components using the relative MHC binding affinity of each neoantigen to its wild type

243 ticle, we show that their emergence required MHC class II and CD40/CD40L interactions.

244 nd unfolded proteins bind to hIRE1alpha LD's MHC-like groove and induce allosteric changes that lead

245 he other hand, in gels made with added salt, MHC polymerization occurred, as evidenced by the electro

246 Self-MHC-I also "licenses" NK cells to become responsive to a

247 d decreased presentation of allopeptide+self-MHC complexes, along with increased PD-L1, on plasmacyto

248 whereas those responding to allopeptide+self-MHC did not.

249 hat inhibit killing of cells expressing self-MHC-I.

250 MV-based vaccine vectors expressing a single MHC class I-restricted high-avidity epitope provided str

251 The combination of six MHC-I alleles each individual carries defines the sub-pe

252 re passively transferred with donor-specific MHC I antibodies, mTOR inhibition significantly reduced

253 were screened using M.tuberculosis-specific MHC class II tetramers.

254 dictating the internalization and subsequent MHC class I (MHC I) display of extracellular Ags.

255 notherapy with DFTD cells expressing surface MHC-I corresponded with effective anti-tumour responses.

256 ch mechanism entails the transfer of surface MHC-self peptide complexes from medullary thymic epithel

257 MHC-Ia and MHC-II, our understanding of TCR/MHC-Ib interactions is very limited.

258 on average, 11 to 32% more efficiently than MHC-B.

259 s to T cell killing by mechanisms other than MHC upregulation.

260 However, there is also evidence that MHC restriction can be imposed on the TCR repertoire dur

261 We observed that MHC-class I acquisition by recipient DCs occurs for at l

262 Immunohistological analyses reveal that MHC-matching reduces the immune response by suppressing

263 itopes in CFP-10 were characterized, and the MHC class II alleles restricting them were determined.

264 l of the recognition of HIV infection by the MHC class I pathway.

265 that respond to glycolipids presented by the MHC class Ib molecule CD1d and are rapidly activated to

266 In contrast, the MHC stable insulin mimetope (InsB9-23 R22E) efficiently

267 Here, we defined the MHC class II alleles for immunodominant Gag CD4(+) T cel

268 both in vitro and in vivo, which defines the MHC class I-LILRB1 signaling axis as an important regula

269 ei GAP5040-48 epitope in mice expressing the MHC class I allele H-2D(b).

270 ical shift effects in sites removed from the MHC-binding site.

271 ity peptides onto MHC I is a key step in the MHC I antigen presentation pathway.

272 e further fine-mapped the association in the MHC to a region of about 50 kilo base pairs, down from 1

273 early endosomes and proper sorting into the MHC class II antigen-presenting compartment (MIIC).

274 Notoriously, the MHC region has been intractable to high-throughput analy

275 the C terminus rather than the center of the MHC alpha1 helix for JM22.

276 We show that expression of the MHC class I genes is downregulated in HPV-positive kerat

277 ing EV biogenesis, no obvious editing of the MHC class I immunopeptidome occurs.

278 the sequence and structural diversity of the MHC region shows the approach accurately determines the

279 For example, expression of the MHC-II Ealpha:Ebeta complex potently protects nonobese d

280 roni-significant druggable genes outside the MHC, and 128 FDR-significant biological pathways related

281 In different macaque species, the MHC A2*05 gene is present in abundance, and its gene pro

282 and traffics rapidly but transiently to the MHC class II loading compartment, as does Ag conjugated

283 In comparison to the MHC class II region in other mammals, the corresponding

284 te at Nef position 9 that contributes to the MHC-B downregulation function in HIV-1 subtype C and sho

285 ot" and demonstrate its role, along with the MHC, in directing the specificity of allorecognition.

286 Polymorphisms located within the MHC have been linked to many disease outcomes by mechani

287 s of T1D and RA were also located within the MHC region.

288 perform this function because they use their MHC-I molecules to exclusively present peptides derived

289 Thus, MHC-E is functionally conserved among humans, RM, and MC

290 r different inherent V-segment affinities to MHC II.

291 gE complex uptake by B cells directed Ags to MHC class II-rich compartments.

292 s-present cell corpse-associated antigens to MHC class I-restricted T cells, a property that was asso

293 Peptide binding to MHC molecules is the single most selective step in the A

294 eptors (TCRs) to recognize peptides bound to MHC molecules (pMHCs) on antigen-presenting cells (APCs)

295 CD8 T cells in the form of peptides bound to MHC-I molecules.

296 rent T cell receptor beta chains and various MHC alleles, we show that positive selection-induced MHC

297 BALB/c mice injected with viable MHC-incompatible 3F7.A10 hybridoma cells grown in serum-

298 es to high-affinity recognition of the viral MHC-I mimic UL18 and a docking strategy that relies on c

299 mount of information on how TCRs engage with MHC-Ia and MHC-II, our understanding of TCR/MHC-Ib inter

300 HDM sensitization was performed in mice with MHC class II expression restricted to the B-cell lineage