ライフサイエンスコーパス: MHC class

1 hifting study demonstrated that induction of MHC class E and II-restricted CD8+ T cells was associate

2 Deficiency of beta2m-dependent MHC class I (but not MHC class II) molecules led to sign

3 We therefore conditionally removed MHC class I (MHC I) from likely cellular targets in anti

4 ause of a reduced ability of DCs to generate MHC class I (MHC I) peptide complexes for cross-presente

5 Myocytes express low levels of MHC class I (MHC I), perhaps influencing the ability of

6 They rely on MHC class I (MHC I)-specific self-receptors to identify

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

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

9 Loss of MHC class I (MHC-I) antigen presentation in cancer cells

10 Consequently, progressing tumors are often MHC class I (MHC-I) low and express immune inhibitory mo

11 nhibitory ligands on target cells, including MHC class I (MHC-I) molecules and other MHC-I-independen

12 ll studied, its impact on the processing and MHC class I (MHC-I) presentation of epitopes and immune

13 are thought to kill cells that down-regulate MHC class I (MHC-I) through "missing-self" recognition.

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

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

16 gain of ThPOK function redirects MHCII- and MHC class I (MHCI)-signaled thymocytes into the CD8 cyto

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

18 ng short virus-derived peptides presented by MHC class I (pMHCI) on the surface of infected cells.

19 Ex vivo HCV MHC class I + II tetramer staining and bead-enrichment w

20 The MHC class I Ag presentation pathway in melanoma cells ha

21 ta2M and HLA in human macrophages as well as MHC class I Ag presentation suppressed by ESAT-6 in peri

22 racts with beta2M, causing downregulation of MHC class I Ag presentation, which could be one of the m

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

24 ptide epitopes is possible for virtually all MHC class I allotypes; in comparison, current MHC class

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

26 s effector, AKT, increased the expression of MHC Class I and CD80 on tumor cells.

27 ment: immune system processes (specifically, MHC class I and class II genes), responses to stimuli, a

28 The study of peptides presented by MHC class I and class II molecules is limited by the nee

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

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

31 IL2rg) (null) (NSG) strains that lack murine MHC class I and II [NSG-beta-2-microglobulin ( B2M) (nul

32 d mononuclear cells in NSG mice deficient in MHC class I and II expression.

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

34 AKI model to investigate the role of various MHC class I and II molecules in regulating kidney DN T c

35 nkey cells and functioned as an adjuvant for MHC class I and II presentation in T cell hybridomas.

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

37 , distinguishing it from its human homologue MHC class I antigen E (HLA-E).

38 inding to endocytic vesicle damage to permit MHC class I antigen presentation of exogenous antigens a

39 The MHC class I antigen presentation system enables T cell i

40 elated with genes involved in IFN signaling, MHC class I antigen presentation, and immune system path

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

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

43 validated 35 predicted peptides to be strong MHC class I binders through direct binding of predicted

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

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

46 We characterized MHC class I exon 2 and exon 3, and neutral diversity (mi

47 une disorders in which pathobiology, ectopic MHC class I expression, and IP collapse play an importan

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

49 umor growth in xenograft models and restored MHC class I expression.

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

51 rrect; the correct citations are as follows: MHC class I free heavy chain(22); HLA-B5802(34); I-E(k)

52 th peptides (i.e. 8-10-mers) to fit into the MHC class I groove.

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

54 t outperforms the state-of-the-art models in MHC Class I ligand prediction.

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

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

57 ell receptor restricted to the non-classical MHC class I molecule MR1 presenting bacterial ligands.

58 iRNAs and the macaque placental nonclassical MHC class I molecule, Mamu-AG.

59 binding of four common Indian rhesus macaque MHC class I molecules (Mamu-A1*001, -A1*002, -B*008, and

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

61 It is therefore intriguing that MHC class I molecules can present N-terminally extended

62 presentation of pathogen-derived peptides on MHC class I molecules is essential for the initiation of

63 ave reduced expression of Nlrc5 and multiple MHC class I molecules that serve to protect cells from N

64 des generated by proteasomes are loaded onto MHC class I molecules to stimulate CD8 T cell responses,

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

66 novo presentation of TE-derived peptides on MHC class I molecules.

67 of their unique ability to bind many common MHC class I molecules.

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

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

70 e immune responses through interactions with MHC class I molecules.

71 or responses to whole Ag were independent of MHC class I on EVs and hypothesized that multiple inject

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

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

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

75 peptide binding affinity prediction to score MHC class I peptide presentation.

76 In particular, MHC class I prediction tools have matured to a point whe

77 MHC class I presentation of short peptides enables CD8(+

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

79 ssibility that in context-specific settings, MHC class I proteins presenting microbial peptides influ

80 apes the repertoire of peptides presented by MHC class I to CD8 T cells, influences other aspects of

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

82 r immunogenicity by increasing calreticulin, MHC class I, antigen presentation and T-cell infiltratio

83 Higher individual diversity of MHC class I, but not class II, was associated with small

84 hose of most other Nef substrates, including MHC class I, CD3, and CD4 but overlaps with the site for

85 locks interferon-gamma-mediated induction of MHC class I, implicating suppressed antigen presentation

86 ics the natural activating ligand of LILRB1, MHC class I, in its LILRB1-binding mode.

87 onents of surface immune recognition such as MHC class I, may be especially confounded.

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

89 stence of an alternative secretory route for MHC class I, which will be worthy of further studies.

90 in at conserved sites in both representative MHC class I- and class II-restricted TCRs, and that thes

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

92 Donor MHC class I- and MHC class II-specific IgE was found on

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

94 dc1(-/-) NK cells are hyporesponsive against MHC class I-deficient cell targets in vitro and in vivo,

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

96 to islet allografts in 5 of 5 nonsensitized, MHC class I-disparate, and one MHC class II DRB allele-m

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

98 y major histocompatibility complex (MHC) and MHC class I-like molecules.

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

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

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

102 ized by many bacteria and fungi presented by MHC class I-related MR1 molecules.

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

104 most human cancer types via the monomorphic MHC class I-related protein, MR1, while remaining inert

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

106 stic of helped primary CTLs upon recall with MHC class I-restricted antigens, likely due to epigeneti

107 We previously showed that an MHC class I-restricted epitope of myelin basic protein (

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

109 nocytogenes-based vector to express a single MHC class I-restricted immune dominant peptide, E294-302

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

111 response that is nonoverlapping with that of MHC class I-restricted neoantigens and therefore needs t

112 pathway of cross-presentation, which allows MHC class I-restricted presentation of peptides derived

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

114 Introduction of an MHC class I-restricted TCR in PSCs produced naive, antig

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

116 ng OPCs by inducing the immunoproteasome and MHC class I.

117 ced by cotreatment with antibodies targeting MHC class I.

118 lizumab, an anti-CCR4 mAb, or a mAb blocking MHC class I.

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

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

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

122 ypt base columnar ISCs, which expressed both MHC classes I and II.

123 with their major histocompatibility complex (MHC) class I (or HLA class I [HLA-I]) ligands.

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

125 icity when major histocompatibility complex (MHC) class I and II genes are inactivated and CD47 is ov

126 fy LASV GP major histocompatibility complex (MHC) class I and II T-cell epitopes.

127 endritic cell (DC) major histocompatibility (MHC) class I and MHC class II--strongly induces T(H) 1 i

128 and lower major histocompatibility complex (MHC) class I gene expression.

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

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

131 regulates major histocompatibility complex (MHC) class I molecule expression.

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

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

134 n SWATH-MS major histocompatibility complex (MHC) class I proteins were highly upregulated at 24 h, w

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

136 as part of major histocompatibility complex (MHC) class I, suggesting an opportunity for targeting th

137 s, whereas major histocompatibility complex (MHC) class I, which can also suppress phagocytosis, is u

138 udies with major histocompatibility complex (MHC) class I- and class II-deficient splenocytes showed

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

140 FcRn), the major histocompatibility complex (MHC) class I-like Fc-receptor, transports immunoglobulin

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

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

143 ntation by major histocompatibility complex (MHC) class I.

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

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

146 The MHC-class-I-like protein of the FcRn heterodimer is enco

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

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

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

150 endritic cells and major histocompatibility (MHC) class Ia molecules.

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

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

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

154 schemia storage had increased levels of anti-MHC class II (but not class I) donor-specific antibodies

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

156 Mice with adipocyte loss of MHC class II (MHC II) are more insulin sensitive.

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

158 after challenge, endothelial cells expressed MHC class II (MHC II).

159 HC class I allotypes; in comparison, current MHC class II (MHC-II) predictors are less mature.

160 even death, elucidating the requirements for MHC class II (MHC-II) processing and presentation of pox

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

162 ase development was dependent on loss of the MHC class II (MHCII) antigen-presenting complex on DCs a

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

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

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

166 MHC class II (MHCII) expression is usually restricted to

167 MHC class II (MHCII) molecules are cell surface glycopro

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

169 reviously determined that TNBC patients with MHC class II (MHCII) pathway expression in their tumors

170 Expression of MHC class II (MHCII) was not restricted to these specifi

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

172 signaling is critical for ThPOK induction in MHC class II (MHCII)-signaled thymocytes leading to the

173 nella enterica effector SteD depletes mature MHC class II (mMHCII) molecules from the surface of infe

174 s following TCR binding to microbial peptide:MHC class II (p:MHCII) complexes on dendritic cells (DCs

175 However, the clinical significance of the MHC class II Ag presentation pathway in melanoma cells i

176 hese studies support a role for GILT and the MHC class II Ag presentation pathway in melanoma outcome

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

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

179 i-MPO autoreactivity in the context of three MHC class II allomorphs.

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

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

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

183 -2, CCL-3, CCL-5, IL-6) as well as decreased MHC class II and costimulatory marker (CD80/86) expressi

184 riptome and indirect specificity for matched MHC class II and mismatched class I peptides.

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

186 identified the first molecular link between MHC class II and the onset of type 1 diabetes.

187 ptive transfer of sera containing anti-donor MHC class II antibodies or mAbs against donor MHC class

188 ntagonist FTY720 specifically inhibited anti-MHC class II antibody production and abrogated macrophag

189 eration of donor-specific antibodies against MHC class II antigens.

190 TDM downregulated MHC class II cell surface expression and impaired T cell

191 and suggests that targeting the self-peptide:MHC class II complex might limit autoimmunity arising fr

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

193 olecules: antigenic peptide binding, peptide-MHC class II complex stability, beta167-169 RGD loop, T-

194 cell system that endogenously expresses the MHC class II complex.

195 ted with a mAb targeting the insulin peptide:MHC class II complex.

196 rred females lacking the DAB*d allele at the MHC class II DAB locus, which had higher average body ma

197 MHC class II deficiency is a rare, but life-threatening,

198 We analyzed the outcome of 25 patients with MHC class II deficiency undergoing first HCT at Great No

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

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

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

202 onsensitized, MHC class I-disparate, and one MHC class II DRB allele-matched rhesus macaques.

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

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

205 Thus, MHC class II expression by IECs in the ileum initiates l

206 r, this work uncovers an unexpected role for MHC class II expression by keratinocytes in the control

207 addition, GM-CSF IRF4 signaling upregulated MHC class II expression in ZIP macrophages and bone marr

208 ssed in benign melanocytes of nevi, GILT and MHC class II expression is induced in malignant melanocy

209 MHC class II expression on IECs was absent from mice def

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

211 We observed that MCs increased their MHC class II expression under hyperlipidemic conditions

212 tably, IL-22-mediated keratinocyte-intrinsic MHC class II expression was required for the selective a

213 or cell line that endogenously expresses the MHC class II gene, HLA-DR.

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

215 ilized by HCMV to decrease the expression of MHC class II in a relevant cell system that endogenously

216 investigated the impact of HCMV infection on MHC class II in Kasumi-3 cells, a myeloid-progenitor cel

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

218 The MHC class II invariant chain (Ii) has been used as an ad

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

220 -SE and XL9-SE are situated within the human MHC class II locus between the HLA-DRB1 and HLA-DQA1 gen

221 d independent association with the principal MHC class II locus from previous GWAS, represented by rs

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

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

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

225 in gene knockout mice lacking either TCRs or MHC class II molecules on B cells.

226 showed that MCs can present Ags in vivo via MHC class II molecules.

227 Lack of MHC class II on DCs also resulted in upregulation of inh

228 tact, there was substantial variation in the MHC class II pathway in the The Cancer Genome Atlas mela

229 rast to healthy skin specimens, in which the MHC class II pathway was nearly uniformly expressed and

230 Both an active and intact MHC class II pathway were associated with improved overa

231 IEC-specific deletion of MHC class II prevented the initiation of lethal GVHD in

232 eins were highly upregulated at 24 h, whilst MHC class II proteins exhibited comparatively fewer chan

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

234 set subgroup we found novel association with MHC class II region indel rs145954018, and independent a

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

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

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

238 HC class II antibodies or mAbs against donor MHC class II restored early glomerular macrophage infilt

239 hed chlamydia-specific CD8 T-cell clones are MHC class II restricted.

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

241 responses were longitudinally analyzed using MHC class II tetramer technology, multicolor flow cytome

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

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

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

245 IL-12/23p40 neutralization prevented MHC class II upregulation on IECs and initiation of leth

246 MHC class II was expressed on intestinal epithelial cell

247 crophages and by inducing differentiation of MHC class II(+) macrophages with enhanced l-Arginase act

248 revealed the identity of this B220(+)CD11c(+)MHC class II(+)NK1.1(+) population as precursors to matu

249 Canine hypodense MHC class II(-)CD5(-)CD21(-)CD11b(+) cells can be subdiv

250 ary and sufficient for induction of CD11c(+) MHC class II(hi) dendritic cells that are implicated in

251 from a CD206(+) MHC class II(lo) to CD206(-) MHC class II(hi) phenotype that normally occurs in the p

252 dent with their polarization from a CD206(+) MHC class II(lo) to CD206(-) MHC class II(hi) phenotype

253 osinophil infiltration (CD45(+)CD11c(-)Gr1(-)MHC class II(lo)SiglecF(+) eosinophils at 1.2 +/- 0.34%

254 ncy of beta2m-dependent MHC class I (but not MHC class II) molecules led to significant reduction in

255 Expression of CD206, TLR2, CD16/CD32, MHC class II, and CD86 was higher in CD11c(+) CD11b(+) A

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

257 ) major histocompatibility (MHC) class I and MHC class II--strongly induces T(H) 1 immune polarizatio

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

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

260 (+) T cells can kill autologous tumors in an MHC class II-dependent fashion and are suppressed by reg

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

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

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

264 rejection is accelerated in KO recipients of MHC class II-mismatched B6.C-H-2(bm12) heart transplants

265 Resulting MHC class II-reactive donor-specific antibodies are esse

266 In addition, the expression of MHC class II-restricted antigens by tumour cells is requ

267 The MHC class II-restricted CD8 T cells may play an importan

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

269 d mutated C-terminal binding protein 1 in an MHC class II-restricted manner.

270 These findings suggest that MHC class II-restricted neoantigens have a key function

271 In the absence of HDAC3, MHC Class II-restricted OT-II thymocytes are redirected

272 somal thiol reductase (GILT) is critical for MHC class II-restricted presentation of disulfide bond-c

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

274 somal thiol reductase (GILT) is critical for MHC class II-restricted presentation of multiple melanom

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

276 The diversion of MHC class II-restricted thymocytes into the regulatory T

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

278 Donor MHC class I- and MHC class II-specific IgE was found on acute rejection o

279 xpression of the IFN-gamma receptor, but not MHC class II.

280 d the majority of PH expressed MHC-E but not MHC class II.

281 HLA-DM (DM), a peptide exchange catalyst for MHC class II.

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

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

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

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

286 cells and major histocompatibility complex (MHC) class II molecules are essential for protective imm

287 ot express major histocompatibility complex (MHC) class II molecules.

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

289 ells or of major histocompatibility complex (MHC) class II on intestinal epithelial cells prevented C

290 levels of major histocompatibility complex (MHC) class II proteins, which are upregulated upon expos

291 within the major histocompatibility complex (MHC) class II region contributes disproportionately more

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

293 y that the major histocompatibility complex (MHC) class II transactivator (CIITA) has antiviral activ

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

295 with SIEC major histocompatibility complex (MHC) class II, which is diurnally modulated by distinct

296 context of major histocompatibility complex (MHC) class II.

297 re presented to CD4(+) and CD8(+) T-cells by MHC class-II and I, respectively.

298 hages, CD4(+) and CD8(+) T cells, and lesion MHC class-II expression, CD31(+) microvessel growth, and

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

300 e also highlighting the complex, potentially MHC class-specific mechanisms by which autoreactivity ma