ライフサイエンスコーパス: MHC

1 MHC class II (MHC II) displays peptides at the cell surf

2 MHC molecules come in two main variants: MHC Class I (MH

3 MHC-I and MHC-II affect antibody isotype switching, sinc

4 MHC-I predominantly present peptides derived from intrac

5 MHC-I-bound peptides originate from protein degradation

6 MHC-II on alveolar type-II (AT-II) cells is associated w

7 C57BL/6 mice, thereby conditionally ablating MHC class I-restricted Ag presentation in targeted APC s

8 and B12A did not exhibit preference against MHC-restriction.

9 uced reactivity to both self- and allogeneic MHC II.

10 n both syngenic MHC-matched and in allogenic MHC-mismatched studies as C57BL/6 (H-2(b)) and BALB/cBy

11 (alpha- myosin heavy chain) promoter (alpha MHC JunD(tg)) were protected against hyperglycemia-induc

12 pecific overexpression of JunD via the alpha MHC (alpha- myosin heavy chain) promoter (alpha MHC JunD

13 onses were examined in two models of altered MHC II ubiquitination: MHCIIKR(KI) (/KI) mice that expre

14 Although MHC II is mainly produced by professional antigen-presen

15 a-1(b) We also demonstrate a hierarchy among MHC-Ib proteins with respect to CD8alphaalpha binding, i

16 ar origin contribute to Treg expansion in an MHC-II-dependent manner in TNF-alpha-mediated IDLA.

17 ualize the dynamics of OX40 expression in an MHC-mismatch mouse model of acute GvHD using OX40-immuno

18 e data provide direct mechanisms by which an MHC-II SE contributes to expression of the locus and sug

19 CXCR-2 and MHC-II colocalization was observed in inflamed lung tiss

20 predictions trained on both MHC binding and MHC ligand elution data (NetMHCPan-4.0 and MHCFlurry).

21 ssential for proper folding of HFE, CD1, and MHC class I and their surface expression.

22 l subset is activated in a TCR-dependent and MHC-unrestricted fashion by so-called phosphoantigens (P

23 t linkage disequilibrium between MHC-DRB and MHC-DOB, suggesting that these loci are unlikely to be c

24 bcutaneous models, alongside similar GD2 and MHC class I expression.

25 MHC-I and MHC-II affect antibody isotype switching, since both PIV

26 ry LCs are robustly programmed for MHC-I and MHC-II antigen presentation.

27 edict binding between peptides and MHC-I and MHC-II, respectively.

28 n two main variants: MHC Class I (MHC-I) and MHC Class II (MHC-II).

29 We sequenced MHC-DRB exon 2 (IIa) and MHC-DOB exon 2 (IIb) on the MiSeq platform from an enclo

30 tching, since both PIV-vaccinated B2m KO and MHC-II KO mice produced less Coxiella-specific IgG than

31 ell receptor of CD4-positive lymphocytes and MHC II on antigen-presenting cells.

32 ated to predict binding between peptides and MHC-I and MHC-II, respectively.

33 tein modification/degradation, ER stress and MHC class I, may expand antigens presented by beta cells

34 at also includes critical variables, such as MHC and T cell receptor repertoire, is needed.

35 Because MHC-II restricted CD4(+) T cells control and orchestrate

36 In both cases, the binding between MHC and antigenic peptides is the most selective step in

37 o significant linkage disequilibrium between MHC-DRB and MHC-DOB, suggesting that these loci are unli

38 a mechanism that ensures the overlap between MHC class I epitopes presented directly or cross-present

39 The relationships between MHC isoforms, calpain systems and meat quality character

40 considering both peptides predicted to bind MHC or experimentally eluted from infected cells, making

41 al network-based predictions trained on both MHC binding and MHC ligand elution data (NetMHCPan-4.0 a

42 on of microbial riboflavin metabolite Ags by MHC class Ib-related (MR1) molecules.

43 ay and the converter that are encoded for by MHC alternative exons 9 and 11, respectively, directly c

44 cenarios of allergen antigen presentation by MHC-I-like molecules to unconventional T cells, the hall

45 ifying tumour-specific peptides presented by MHC class I molecules and the ability of tumour cells to

46 D8(+) T cells unconventionally restricted by MHC class II and the nonclassical MHC-E molecule in RM.

47 BCG infection increased expression of CD54, MHC Class I and II molecules in endothelial but not epit

48 question is whether the myosin heavy chain (MHC) isoforms alone account for these distinct physiolog

49 bit transcription of the myosin heavy chain (MHC) protein family.

50 cells present overlapping sets of Chlamydia-MHC class II epitopes to link inductive and effector pha

51 alleles), as was expected of a non-classical MHC gene.

52 We fine-mapped the classical MHC (chr6: 29.6-33.1 Mb), imputing 216 human leukocyte a

53 immune response guided by the locally common MHC alleles.

54 the three major histocompatibility complex (MHC) class I genes (human leukocyte antigen A [HLA-A], -

55 encoded by major histocompatibility complex (MHC) class I loci in humans.

56 Major Histocompatibility Complex (MHC) class I molecules selectively bind peptides for pre

57 amilies of major histocompatibility complex (MHC) class I, MHC class II and alphabeta T cell receptor

58 identified major histocompatibility complex (MHC) class I-binding epitopes in the tail length tape me

59 ls and the major histocompatibility complex (MHC) class I-primed CD8(+) T cell response.

60 context of major histocompatibility complex (MHC) class Ia and class II molecules and provide anti-mi

61 bined with major histocompatibility complex (MHC) class II tetramers to interrogate endogenous, Salmo

62 in a given major histocompatibility complex (MHC) context.

63 ele of the major histocompatibility complex (MHC) I gene HLA-B in the occurrence of penicillin allerg

64 ons in the major histocompatibility complex (MHC) locus, an association that in SLE and Sjogren's syn

65 (class-Ib) major histocompatibility complex (MHC) molecules (MHC-Ibs) have recently been identified a

66 to class I major histocompatibility complex (MHC) molecules in the endoplasmic reticulum (ER) and rer

67 turing the Major Histocompatibility Complex (MHC) of a random sample.The application provides users w

68 d class II major histocompatibility complex (MHC) pathways.

69 igen (HLA)/major histocompatibility complex (MHC) proteins limit successful transplantation and trans

70 esented by major histocompatibility complex (MHC) proteins to T cells.

71 diversity, major histocompatibility complex (MHC) variants, satellite DNAs, and segmental duplication

72 1 class Ib major histocompatibility complex (MHC), a mouse homolog of human leukocyte antigen-E (HLA-

73 eful - the Major Histocompatibility Complex (MHC).

74 class I major histocompatibility complexes (MHC) play a critical role in immune cell recognition and

75 nding to major histocompatibility complexes (MHCs) is a central component of the immune system, and u

76 However, current MHC-binding prediction methods lack an analysis of the m

77 -2, CCL-3, CCL-5, IL-6) as well as decreased MHC class II and costimulatory marker (CD80/86) expressi

78 m signaling effects and on strain-dependent, MHC class II disparity with naive T cells, which may exp

79 H-2(b)) and BALB/cBy (H-2(d)) have disparate MHC haplotypes.

80 ZH2 and thymidylate synthase, enhanced DLBCL MHC-I presentation.

81 recipient or blocking PIR-A binding to donor MHC-I molecules blocks memory and attenuates kidney and

82 f model proteins by RQC results in efficient MHC-I presentation, independent of their intrinsic foldi

83 s, and increases the levels of peptide-empty MHC-I conformers that can be loaded with peptide in this

84 tide-depleted environments stabilizing empty MHC I and impeding peptide rebinding.

85 HLA class II alleles encode MHC proteins on antigen-presenting cells, which function

86 cell response is understudied in endogenous MHC class II-expressing cells, largely because the popul

87 is understudied in the context of endogenous MHC class II regulation.

88 Restoration of endothelial MHC I rendered MHC I-deficient mice susceptible to lung

89 or studying HCMV do not endogenously express MHC class II.

90 s I (MHC-I) Ags via stochastically expressed MHC-I-specific inhibitory receptors that prevent NK cell

91 molecules or also to ubiquitously expressed MHC-Ib molecules.

92 rogenitor cell model endogenously expressing MHC class II (HLA-DR), this study shows that HCMV decrea

93 GILT facilitated MHC class II-restricted presentation of endogenous TRP1

94 Cs in particular, preferentially facilitates MHC class II-restricted presentation, negative selection

95 ational selection mechanism that facilitates MHC-I recruitment into the complex.

96 ctions and to previously published findings, MHC heterozygosity was not related to any of the psychol

97 ntly, predicted peptide binding affinity for MHC-I is often the major criterion for prioritizing neoa

98 ital has significantly improved outcomes for MHC class II deficiency.

99 an migratory LCs are robustly programmed for MHC-I and MHC-II antigen presentation.

100 aminopeptidase Erap1, which are required for MHC-I trafficking to the cell surface.

101 H8), the E3 ubiquitin ligase responsible for MHC II ubiquitination specifically in thymic epithelial

102 ted the Valphabeta-domain is responsible for MHC-independent B12A recognition of its ligand.

103 o further analyze immunological subjects for MHC homo-to-hetero iPSC-based transplantation.

104 D8 T cell responses restricted by these four MHC molecules have already been identified in SIVmac239,

105 e showed an increase in IL-1beta, IFN-gamma, MHC II, and Ctss mRNA transcripts compared with young wi

106 In this study, we have examined how MHC II ubiquitination impacts the composition and functi

107 rotein efficiently redirects the U21/class I MHC complex to the lysosomal compartment is poorly under

108 ult in sorting of the oligomeric U21/class I MHC complexes to Golgi--derived quality control carriers

109 of forming oligomeric complexes with class I MHC molecules that result in sorting of the oligomeric U

110 Nonclassical class I MHC-like molecules are ligands for several unconventiona

111 on major histocompatibility complex class I (MHC I) molecules loaded with peptides.

112 of major histocompatibility complex class I (MHC I) proteins, from their synthesis in the endoplasmic

113 NK cells recognize MHC class I (MHC-I) Ags via stochastically expressed MHC-I-specific i

114 ules come in two main variants: MHC Class I (MHC-I) and MHC Class II (MHC-II).

115 regulating major histocompatibility class I (MHC-I) expression to evade killing by cytotoxic T lympho

116 rt major histocompatibility complex class I (MHC-I) peptide presentation to evade CD8(+) T cell immun

117 he major histocompatibility complex class I (MHC-I), which has been implicated in resistance to immun

118 he major histocompatibility complex class-I (MHC-I) peptide-loading complex (PLC) is a cornerstone of

119 major histocompatibility complex classes I (MHC-I) and II (MHC-II) (mainly through the endogenous pa

120 or histocompatibility complex (MHC) class I, MHC class II and alphabeta T cell receptors, the antigen

121 hat harbors a point mutation in the class Ib MHC molecule Qa-1, which disrupts Qa-1 binding to the T

122 t on pDC viability, immaturity, and class II MHC mismatch and blocked by MEK/ERK and NFkappaB inhibit

123 patibility complex classes I (MHC-I) and II (MHC-II) (mainly through the endogenous pathway) and the

124 l major histocompatibility complex class II (MHC II) accessory molecule mainly expressed in the thymi

125 MHC class II (MHC II) displays peptides at the cell surface, a process

126 e major histocompatibility complex class II (MHC II)-CD4 immunologic synapse is classically described

127 e major histocompatibility complex class II (MHC-II) molecule.

128 iants: MHC Class I (MHC-I) and MHC Class II (MHC-II).

129 impairs major histocompatibility complex II (MHC-II) presentation.

130 oci of the immunopositive and immunonegative MHC-I neoantigens have distinct spatial distribution pat

131 ide-MHC-II binding data as well as improving MHC-II prediction tools.

132 and male patients, despite no differences in MHC genotype.

133 vidence that DN T cells can differentiate in MHC-deficient mice.

134 This region is rich in MHC-IB genes, several of which interact with inhibitory

135 andscape, transactivated NK cells, increased MHC class II expression on macrophages, and restored del

136 Individual MHC genotype constrains the mutational landscape during

137 Pharmacological inhibitors of Nef-induced MHC-I down-regulation restore the adaptive immune respon

138 192 SIVmac239 peptides with the most intense MHC binding signals in our experiment.

139 Interestingly, MHC-II and CD4 deficiencies were not equivalent in terms

140 tissue (skin) grafts were transplanted into MHC-heterozygous recipients.

141 However, in this largely MHC-class-I-negative tumor, the mechanism of action of a

142 ecific receptor(s) on other cells, much like MHC molecules and T cell receptors (TCRs).

143 our results suggest that a loss of NOD-LNSC MHC-independent suppressive mechanisms may contribute to

144 a conformation reminiscent of antigen-loaded MHC-I.

145 t of a polyubiquitin chain to peptide-loaded MHC II, promoting its traffic away from the plasma membr

146 cytometry in combination with peptide-loaded MHC tetramer staining.

147 ogen control and argue that the normally low MHC I expression in skeletal muscle is host protective b

148 of this diurnally regulated diet-microbiome-MHC class II-IL-10-epithelial barrier axis by circadian

149 ted in reduced TNF production and microglial MHC-II and improved neurocognitive activity.

150 nd that under TNFRp55 deficiency, migratory (MHC(high)CD11c(+)) DCs increased significantly in RLN.

151 histocompatibility complex (MHC) molecules (MHC-Ibs) have recently been identified as ligands for th

152 Throughout the body, T cells monitor MHC-bound ligands expressed on the surface of essentiall

153 otein antigens in the context of monomorphic MHC class I-like molecules.

154 The antigen-presenting molecule MR1 (MHC class I-related protein 1) presents metabolite antig

155 compounded effects and nearly twice as much MHC-II based selection.

156 of binding to the well-characterized murine MHC allele H-2D(b) are known, by applying thresholds for

157 temically dominant effect of skeletal muscle MHC expression on maintaining T cell function and pathog

158 Inducible enhancement of skeletal muscle MHC I in mice during the first 20 d of T. cruzi infectio

159 MHCIIKR(KI) (/KI) mice that express a mutant MHC II unable to be ubiquitinated or mice that lack memb

160 ll recognition, whereas substitutions at non-MHC anchor positions were neutral, except for one epitop

161 linked gammadelta TCR recognizing intact non-MHC proteins on the opposing cell surface.

162 ble, and their structural recognition of non-MHC ligand remains unknown.

163 Ag presentation via the nonclassical MHC class Ib molecule HLA-E, with nearly complete identi

164 tricted by MHC class II and the nonclassical MHC-E molecule in RM.

165 tebrates, we identified a third nonclassical MHC class I lineage (UDA), which is present in all speci

166 Five novel MHC II tetramers were made using an immunodominant EFYQS

167 PBMC-engrafted NSG, NSG-MHC-DKO, and NSG-SGM3 mice were used to study cytokine r

168 that can be used to improve the accuracy of MHC-II binding prediction algorithms, and potentially en

169 s present alloantigens is via acquisition of MHC-peptide complexes.

170 restored expression of diverse allotypes of MHC-I in Nef-expressing cells and inhibited Nef alleles

171 The availability of MHC-binding prediction tools has been useful in guiding

172 tractive strategy to generate vast bodies of MHC-II binding data at an unprecedented speed and for th

173 his process, Rab39a promotes the delivery of MHC-I molecules from the endoplasmic reticulum (ER) to p

174 nesis by contributing to the derepression of MHC transcription.

175 nd(5) despite the frequent downregulation of MHC-I expression(6-8).

176 unger patients show the strongest effects of MHC-based driver mutation selection, with younger female

177 The first examination of MHC-DOB in white-tailed deer found significantly less po

178 PDAC cells display reduced expression of MHC-I at the cell surface and instead demonstrate predom

179 +) T cells or reducing surface expression of MHC-I.

180 c cells, evidenced by enhanced expression of MHC-II and CD86, and induced a memory T-cell response, a

181 uman LA samples, we found high expression of MHC-II in tumor cells of AT-II cellular origin, which wa

182 that demonstrate improved identification of MHC class II-binding peptides.

183 To date, no structural information of MHC-independent TCRs is available, and their structural

184 ulum, which contributes toward inhibition of MHC class I:beta2M:peptide complex formation.

185 r lymphocytic infiltration, higher levels of MHC II, IFN-gamma, IL-1beta, TNF-alpha, and cathepsin S

186 tion of autophagy restores surface levels of MHC-I and leads to improved antigen presentation, enhanc

187 cluding ICB(4), mutations that cause loss of MHC-I are rarely found(5) despite the frequent downregul

188 tic cells (DCs), as well as up-regulation of MHC class I and down-regulation of checkpoint regulator

189 Lastly, we found that restoration of MHC-I in HIV-infected cells was accompanied by enhanced

190 Via screening of MHC-restricted libraries comprising ~2x10(8) sequence-di

191 y immunoaffinity isolation and sequencing of MHC class I- and II-bound peptides.

192 m AT-II cells, which are the major source of MHC-II.

193 While the general structure of MHC genes is relatively well conserved among mammalian s

194 in immune evasion by selective targeting of MHC-I molecules for degradation, and provide a rationale

195 nd B12A TCR are nearly identical to those of MHC-restricted TCR, including the conformations of CDR1

196 Triggering of MHC molecules by migrating T-cells is a minimal signal c

197 R-2 deficiency inhibited the upregulation of MHC-II on AT-II cells in inflamed lung tissue.

198 ent peptides derived from endocytosed Ags on MHC class I molecules, which is important for activating

199 e that this trimming cannot readily occur on MHC I molecules, but rather only in solution, suggesting

200 mulated by recombinant peptides presented on MHC Ag alone, we show that different inflammatory cytoki

201 However, complexities of selection on MHC genes are simultaneously being revealed that need to

202 ed on machine learning algorithms trained on MHC binding or naturally processed MHC ligand elution da

203 12-mer is highly labile and that apparent on-MHC trimming rates are always slower than that of MHCI-p

204 are CD4(+) or CD8(+) and recognize MHC I- or MHC II-presented antigens, are essential for immune resp

205 ckout mice lacking either functional TCRs or MHC class II molecules on B cells, the liposomal particl

206 LoxP-transgenic mouse system using otherwise MHC class I-deficient C57BL/6 mice, thereby conditionall

207 h major histocompatibility complex pathways (MHC I and II).

208 Here we show that, in PDAC, MHC-I molecules are selectively targeted for lysosomal d

209 Peptide MHC class II-based (pMHCII-based) nanomedicines trigger

210 increase in TCR sensitivity to self-peptide MHC in vivo and an enhanced response to weak agonist pep

211 ell receptors (TCRs) to their target peptide MHC (pMHC) ligands initializes the cell-mediated immune

212 ent on tonic TCR signaling through peptide + MHC class I (MHCI) recognition; however, little is known

213 h different TCRs may interact with a peptide-MHC ligand, but very few will activate.

214 presented here can be applied to any peptide-MHC complex of interest with a structural model as input

215 ed and for the benefit of generating peptide-MHC-II binding data as well as improving MHC-II predicti

216 ringent selection against a narrower peptide-MHC-II context.

217 t an atomically detailed analysis of peptide-MHC binding that can reveal the contributions of any int

218 actions depend on TCR recognition of peptide-MHC molecules; yet the degree of peptide specificity of

219 des and subsequently large bodies of peptide-MHC-II interaction data are key to the solution of this

220 primary T cells resulted in specific peptide-MHC-tetramer binding and reactivity against EBV-LMP2-exp

221 standing the mechanism behind stable peptide-MHC binding will aid the development of immunotherapies.

222 ehensive in silico analysis of viral peptide-MHC class I binding affinity across 145 HLA-A, -B, and -

223 ains, which govern interactions with peptide-MHC complexes.

224 d CD8(+) epitopes were defined, with peptide-MHC pentamer-positive cells displaying the central and e

225 inst ~50% of neoantigens with high predicted MHC-I binding affinity and led to enhanced tumor clearan

226 rained on MHC binding or naturally processed MHC ligand elution data.

227 Protective MHC class I-dependent immune responses require an overla

228 Vbeta) to "horizontally" grab the protruding MHC alpha2-helix.

229 Substitutions of AABA for Cys at putative MHC anchor positions often significantly enhanced T cell

230 t-display-based platform yields high-quality MHC-II-binding peptide datasets that can be used to impr

231 Without Rab39a, MHC-I presentation of intraphagosomal peptides is inhibi

232 ng an anti-CD20 antibody, prior to receiving MHC class I-mismatched (K(d) ) skin.

233 es, including pattern recognition receptors, MHC class II genes, and IFN-gamma-induced GTPases, with

234 ntified human gammadelta T cells recognising MHC-related protein-1 (MR1) via their T cell receptor (T

235 of which are CD4(+) or CD8(+) and recognize MHC I- or MHC II-presented antigens, are essential for i

236 NK cells recognize MHC class I (MHC-I) Ags via stochastically expressed MHC

237 Restoration of endothelial MHC I rendered MHC I-deficient mice susceptible to lung injury.

238 cancer, selective autophagy instead reroutes MHC-I to lysosomes, using the ubiquitin-binding receptor

239 Within these RLN, resident (MHC(int)CD11c(+)) DCs increased on days 14 and 21.

240 A potent Nef inhibitor that restores MHC-I is needed to promote immune-mediated clearance of

241 atures of a restricted component in the self-MHC-II peptidome that caused autoreactivity.

242 We sequenced MHC-DRB exon 2 (IIa) and MHC-DOB exon 2 (IIb) on the MiS

243 ding time or content, or epithelial-specific MHC class II depletion leads to an extensive microbial p

244 CD8alphaalpha binds only to tissue-specific MHC-Ib molecules or also to ubiquitously expressed MHC-I

245 s due to a chromosomal inversion that splits MHC type II genes into two subregions (IIa, IIb).

246 ination is a mechanism that dictates surface MHC II with the attachment of a polyubiquitin chain to p

247 ce for tracking donor cells in both syngenic MHC-matched and in allogenic MHC-mismatched studies as C

248 These results provide proof-of-concept that MHC-E-restricted CD8(+) T cells could be harnessed for t

249 Using DO QTL analysis, we show that MHC-IB reactive NK cells exert positive influence on the

250 Recent studies have shown that MHC class II (MHCII) expression and tumor infiltrating l

251 This suggests that MHC-Ib proteins may be an extended source of CD8alphaalp

252 The MHC-I-linked glycan steers a tapasin loop involved in pe

253 re determined by genetic factors such as the MHC molecules the individual expresses, in parallel to t

254 igand for CD8alphaalpha which also binds the MHC-Ib molecule H2-TL.

255 e by a CD8 T cell response restricted by the MHC class I molecule H-2D(b) The identity and function o

256 e from myelin basic protein presented by the MHC class II molecule HLA-DR4.

257 To investigate the immune response in the MHC homo-to-hetero transplantation, we established a mur

258 These peptides were also found in the MHC-II peptidome of the pancreatic lymph nodes and splee

259 Apart from the well-known cases of the MHC and ABO genes, this study provides the first evidenc

260 nt step toward comprehensive modeling of the MHC class I pathway.

261 HLA molecules of the MHC class II (MHCII) bind and present pathogen-derived p

262 However, viral regulation of the MHC class II-mediated CD4(+) T cell response is understu

263 antigen-binding breadth and expansion of the MHC gene family, associated autoimmunity trade-offs, hit

264 on of the scoop loop to the stability of the MHC I-chaperone complex and to peptide editing.

265 Divergent genomic rearrangements of the MHC II pathway among fully pregnant species were identif

266 thus) displayed loss of several genes of the MHC II pathway while seahorses (Hippocampus) featured a

267 y synergy between the binding pockets of the MHC molecule.

268 have an adaptive immune system based on the MHC and Ig superfamily-based AgR.

269 tes and monocyte-derived cells presented the MHC class I-restricted MBP ligand in the brain compared

270 usly described viral genes that regulate the MHC class II complex or the unique short (US) region of

271 s a central role in the PLC, stabilizing the MHC-I binding groove in a conformation reminiscent of an

272 This suggests that the MHC diversity of the Madagascar populations may have ena

273 nance-based binding assays, we show that the MHC-Ib family furnishes multiple binding partners for mu

274 This suggests that the MHC-II antigen presentation pathway is required for PIV-

275 uccessfully map the UBC-GFP transgene to the MHC locus.

276 iking of deleterious mutations linked to the MHC, geographic subdivision, and adaptive introgression.

277 for selected strongly binding alleles to the MHC-I T-cell epitopes using molecular docking and the co

278 ndings of a chromosomal inversion within the MHC type II gene region in ruminants, and suggests that

279 programs of agonist-signaled cells to their MHC specificity, and identified correspondences between

280 y have a recombination hotspot between these MHC regions similar to that found for Bos taurus.

281 and presentation on the cell surface through MHC class I.

282 microglia in CNS-GVHD, identify the TAK1/TNF/MHC-II axis as a mediator of CNS-GVHD, and provide a TAK

283 ly interfering with their ability to bind to MHC molecules.

284 algorithms for predicting peptide binding to MHC-II proteins have been reported, their performance va

285 issues and display them as peptides bound to MHC-I molecules.

286 reflecting distinct modes of TCR fitting to MHC-II variants.

287 s tissue-dependent persistence was linked to MHC expression.

288 etected previously in the beta chains of two MHC class I-restricted TCRs, thereby revealing a common

289 Recently, we found TNF-alpha upregulated MHC-II in AT-II in vitro.

290 fic, CD8 T cell-derived TCR (AGA1 TCR) using MHC class I yeast display technology.

291 MHC molecules come in two main variants: MHC Class I (MHC-I) and MHC Class II (MHC-II).

292 is of A11 and B12A sequences against various MHC-restricted and -independent TCR sequence repertoires

293 sing and presentation of peptide antigen via MHC class I (PFDR = 0.02).

294 ns known to disrupt antigen presentation via MHC class I.

295 mma ELISpot screening, confirmed by in vitro MHC binding.RESULTSActivated CD4+ T cell frequencies in

296 ponses in diverse situations including where MHC expression is compromised, or where conventional ada

297 Whereas MHC-matched NOD-LNSC significantly reduced G9Calpha(-/-)

298 derived from intracellular proteins, whereas MHC-II predominantly presents peptides from extracellula

299 lished a murine experimental system in which MHC-matched but minor antigen-mismatched tissue (skin) g

300 ormation of cellular protrusions tipped with MHC class I protein.