ライフサイエンスコーパス: class I antigen

1 different forms of hepatocyte-expressed MHC class I antigen.

2 liver produces large amounts of soluble MHC class I antigen.

3 able IgG antibody response against donor MHC class I antigen.

4 ptor, and human histocompatibility leukocyte class I antigen.

5 monomorphic major histocompatibility complex class I antigen.

6 e specific for class II antigens and one for class I antigens.

7 n Ly49I and H2-K(b), H2(s), H2(v), and H2(q) class I antigens.

8 consistently low expression of specific HLA class I antigens.

9 of PKR and major histocompatibility complex class I antigens.

10 and decreased cell surface expression of HLA class I antigens.

11 an Th cells upon specific recognition of MHC class I antigens.

12 class I antigens and to other unrelated HLA class I antigens.

13 recipients are sensitized to mismatched HLA class I antigens.

14 on of major histocompatibility complex (MHC) class I antigens.

15 lability for loading and presentation of HLA class I antigens.

16 the ERAP-mediated processing pathway of MHC class I antigens.

17 g the major histocompatibility complex (MHC) class I antigens.

18 elated to, known KIRs and binds cellular MHC class I antigens.

19 g of cellular major histocompatibility (MHC) class I antigens.

20 ceive negative signals from both H-2d and Kb class I antigens.

21 donor major histocompatibility complex (MHC) class I antigens.

22 b promoter region and down-regulation of HLA class I antigens.

23 binding of known immunogenic SARS-CoV-2 HLA class I antigens.

24 ions (AASs) at specific peptide positions of class I antigens.

25 esponses were directed against the donor HLA-class I antigens.

26 antibodies identified were directed against class I antigens.

27 103 HLA class I epitopes shared by groups of class I antigens.

28 cted sensitization to class II, and possibly class I, antigens.

29 irty-two percent developed dnDSA against HLA class I antigens, 56% developed against class II antigen

30 The potential negative impact of HLA class I antigen abnormalities on the outcome of T cell-b

31 pes contain dominant anchor residues for MHC class I antigen alleles H-2D(b) and H-2K(b), respectivel

32 cause the BB-1-positive fibers expressed MHC-class I antigen and bound to up-regulated counterrecepto

33 Major histocompatibility complex (MHC) class I antigen and Fas/CD95 constitutive surface expres

34 tion were reduced significantly, whereas MHC class I antigen and Fas/CD95 levels were elevated to 2.0

35 tive in CIITA induction, does not induce MHC class I antigen and promoter in response to IFNgamma.

36 oduced both major histocompatibility complex class I antigen and unique tumor antigen loss variants.

37 ls harbor significant cell surface levels of class I antigens and are susceptible to CTL lysis.

38 hibited by monoclonal antibodies against SLA class I antigens and human CD8, which indicates that hum

39 on of major histocompatibility complex (MHC) class I antigens and lack of MHC class II expression.

40 ctivity was directed to one of the donor HLA class I antigens and to other unrelated HLA class I anti

41 ratumoral CD8 T cells, the expression of MHC class I antigen, and the expression of the NY-ESO-1 tumo

42 Major histocompatibility complex (MHC) class I antigens are constitutively expressed yet highly

43 e levels of major histocompatibility complex class I antigens are diminished on tumorigenic adenoviru

44 s) or antibodies (OX18 and OX27) against MHC class I antigens as the second event.

45 d NH2-terminal V(H) sequences are nested MHC class I antigen-binding peptides.

46 terferon not only increased the synthesis of class I antigens but also allowed excess molecules to es

47 ed CMV- and EBV-infected targets sharing HLA class I antigens, but not HLA mismatched targets.

48 yed when grafts were mismatched for only MHC-class I antigens, but ultimately reached the same levels

49 s and major histocompatibility complex (MHC) class I antigens by Nef is believed to be important in A

50 IgG antibodies to HLA class I antigens can cause hyperacute rejection of renal

51 Cytotoxic IgG against class I antigens can contribute to renal dysfunction or

52 D), we recently demonstrated that Abs to MHC class I antigens can induce immune responses to self-ant

53 ets, including cells that poorly express MHC class I antigens, can be lysed.

54 ion can occur on very low levels of the same class I antigen capable of negative selection when expre

55 lpha1 domain of the major histocompatibility class I antigen complex (MHC-I) inhibit receptor interna

56 s I associations suggests that virus-related class I-antigen complexes are not T-cell targets in MS.

57 The reduced surface levels of class I antigens contribute to the tumorigenic potential

58 HLA class I antigen defects are frequently found in malignan

59 iver failure with donor hepatocytes with HLA class I antigen disparate from recipients is clinically

60 stinguishing it from its human homologue MHC class I antigen E (HLA-E).

61 ms of major histocompatibility complex (MHC) class I antigen, each with the potential to induce diffe

62 egulation is triggered by a single donor HLA Class I antigen, either in membrane-bound or soluble for

63 the presence of ELISA-detected IgA anti-HLA class I antigen (ELISA-IgA PRA greater than or equal to

64 e levels of major histocompatibility complex class I antigens enable adenovirus type 12 (Ad12)-transf

65 pate as effector cells, recognizing residual class I antigens expressed by the MHC-deficient grafts.

66 al activities including up-regulation of MHC class I antigen expression and induction of the antivira

67 ulate major histocompatibility complex (MHC) class I antigen expression and may trigger an autoimmune

68 ne with a wild-type beta2m gene restored HLA class I antigen expression and, in Me18105 cells, recogn

69 tigate the mechanisms underlying lack of HLA class I antigen expression by melanoma cell lines Me1810

70 This study investigated whether class I antigen expression impacted relapse-free surviva

71 pha-induced major histocompatibility complex class I antigen expression in mouse L929 cells stably tr

72 ble of inducing antiviral protection and MHC class I antigen expression in several cell types includi

73 This low class I antigen expression is due to a block in class I

74 Human major histocompatibility (MHC) class I antigen expression is important in controlling t

75 C-deficient mice actually do have sufficient class I antigen expression to cause skin graft rejection

76 Interactions between treatment and class I antigen expression were tested.

77 B*2706 and B*2709 during early events in HLA class I antigen expression, and determine if their behav

78 gulation of major histocompatibility complex class I antigen expression, but exhibited impaired induc

79 ization and major histocompatibility complex class I antigen expression.

80 antibodies against class II but not against class I antigens for >30 days and the lack of IgG isotyp

81 the indirect alloresponse to processed donor class I antigen, giving mechanistic insight into the man

82 press a B cell receptor that reacts with MHC class I antigens H-2K(b).

83 Major histocompatibility (MHC) class I antigen (H-2, all haplotypes) expression in thre

84 g NSV encephalitis and demonstrated that MHC class I antigen (H2K/D) was expressed on endothelial cel

85 between expression of > or = two of five HLA class I antigens (HLA-A2, HLA-A28, HLA-B44, HLA-B45, and

86 One class I antigen, HLA-A28, was significantly more common

87 A strong association between an HLA class I antigen, HLA-B51, and Behcet's disease has long

88 Expression of HLA class I antigens, however, is not always associated with

89 jection of recombinant Lewis rat-derived MHC class I antigens in Dark Agouti (DA) rats modulates allo

90 gulation of major histocompatibility complex class I antigens in myositis.

91 rthermore, the evaluation of the role of HLA class I antigens in the interaction of malignant cells w

92 c marrow and MAPCs; such MAPCs expressed MHC class I antigens in tissues.

93 onses using cell lines expressing single-HLA class-I antigens in the presence/absence of PD-1/CTLA-4

94 , (2) the specific unresponsiveness to donor class I antigen induced by a class I-disparate kidney pr

95 fic for the major histocompatibility complex class I antigen Kb, were placed in culture with irradiat

96 These cells recognize and engage MHC class I antigens, leading to allospecific cytolytic resp

97 Class I antigen-level mismatches were associated with wo

98 e to the potential clinical relevance of HLA class I antigen losses in melanoma cells and the scanty

99 levels were influenced by the degree of HLA class I antigen match and donor age.

100 to restenosis and that IgG antibodies to MHC class I antigen may help predict the risk of restenosis

101 h a single class I allele mismatch, a single class I antigen mismatch, or two or more class I mismatc

102 HLA class I antigen mismatches that are serologically detect

103 atients, but not control patients, with more class I antigen mismatches were more likely to have reje

104 associated with more rejection episodes than class I antigen mismatches.

105 interact with classical or non-classical MHC class I antigens of the adaptive immune system, thus fun

106 hypervariable regions of the mismatched HLA class I antigens of the donor.

107 does not affect the transferrin receptor or class I antigens of the major histocompatibility complex

108 with major histocompatibility complex (MHC) class I antigens on lymphoma cells by anti-KIR antibodie

109 pression of major histocompatibility complex class I antigens on subinfundibular follicle epithelium,

110 Relevant expression of MHC class I antigens on the sarcolemma was present in 23 of

111 pression of major histocompatibility complex class I antigens on the surface of adenovirus type 12 (A

112 iferation; however, no effects on either MHC class I antigen or Fas expression was evident.

113 d (2) the infusion of antibodies against MHC class I antigens or the plasma from stored blood.

114 ransport of major histocompatibility complex class I antigens out of the endoplasmic reticulum to the

115 jection of anti-rat CD59 (6D1), anti-rat MHC class I antigen (OX-18), anti-rat Ig (G-16-510E3), or MO

116 ly unrecognized MHC-encoded influence on the class I antigen pathway.

117 Thus, this report demonstrates that: (1) MHC class I antigens play an important role in the pathogene

118 to detect IgG reactivity against soluble HLA class I antigens (PRA-STAT) may allow for the determinat

119 y detecting IgG reactive against soluble HLA class I antigens (% PRA-STAT).

120 ciated with major histocompatibility complex class I antigen presentation and NK cell activation was

121 n-regulates major histocompatibility complex class I antigen presentation and, in the 4T1 syngeneic m

122 Human cytomegalovirus (HCMV) inhibits MHC class I antigen presentation by a sequential multistep p

123 cognate antigen behind the BBB: luminal MHC class I antigen presentation by cerebral endothelium to

124 renal cell carcinoma (RCC), the lack of MHC class I antigen presentation can be attributed to the do

125 ified transcriptional suppression of several class I antigen presentation genes.

126 f tapasin was sufficient to reconstitute MHC class I antigen presentation in insect cells, thus defin

127 -loading control, the quality control of MHC class I antigen presentation includes the restriction of

128 separation of vector delivery and successful class I antigen presentation indicated that T-cell primi

129 companied by coordinate induction of the MHC class I antigen presentation machinery, illustrating an

130 e results demonstrate that the inhibition of class I antigen presentation observed in CMV-infected ce

131 These agents block class I antigen presentation of a model protein, ovalbum

132 ng to endocytic vesicle damage to permit MHC class I antigen presentation of exogenous antigens and t

133 tion from intracellular pathogens that limit class I antigen presentation or diminish CD4 T-cell numb

134 entered the major histocompatibility complex class I antigen presentation pathway and induced mucosal

135 virus gene product K3 (KK3) subverts the MHC class I antigen presentation pathway by downregulating M

136 s the major histocompatibility complex (MHC) class I antigen presentation pathway by inhibiting pepti

137 irect major histocompatibility complex (MHC) class I antigen presentation pathway ensures intracellul

138 The major histocompatibility complex (MHC) class I antigen presentation pathway is a major target o

139 e of delivering heterologous antigens to the class I antigen presentation pathway stimulating immune

140 for delivery by these nanomachines into the class I antigen presentation pathway to stimulate antige

141 ess upregulates the immunoproteasome and MHC class I antigen presentation pathway via cGAS/STING/type

142 r the major histocompatibility complex (MHC) class I antigen presentation pathway, which plays a key

143 t the major histocompatibility complex (MHC) class I antigen presentation pathway.

144 blocks the major histocompatibility complex class I antigen presentation pathway.

145 iple components at various levels in the HLA class I antigen presentation pathway.

146 and essential components involved in the MHC class I antigen presentation pathway.

147 ssing (TAP) plays a critical role in the MHC class I antigen presentation pathway.

148 UGT1 adds a new level of control in the MHC class I antigen presentation pathway.

149 to exploit the late and early stages of the class I antigen presentation pathway.

150 role for HCMV pp71 in disruption of the MHC class I antigen presentation pathway.

151 nous peptides for entry into the classic MHC class I antigen presentation pathway.

152 The major histocompatibility complex class I antigen presentation pathways play pivotal roles

153 onal T cell recognition by rendering the HLA class I antigen presentation system defective.

154 The MHC class I antigen presentation system enables T cell immun

155 cking major histocompatibility complex (MHC) class I antigen presentation to CD8+ T cells.

156 ssing major histocompatibility complex (MHC) class I antigen presentation to cytotoxic T lymphocytes.

157 eficient in major histocompatibility complex class I antigen presentation) were not able to control a

158 ed with genes involved in IFN signaling, MHC class I antigen presentation, and immune system pathways

159 ecialized type of proteasome involved in MHC class I antigen presentation, antiviral adaptive immunit

160 proposed to perform specialized roles in MHC class I antigen presentation, cytokine modulation, and T

161 lobulin (B2M), an essential component of MHC class I antigen presentation, in 29.4% of patients with

162 t increase in other elements involved in MHC class I antigen presentation, including beta-2 microglob

163 AP1 increased the supply of peptides for MHC class I antigen presentation.

164 unction overcame viral interference with MHC class I antigen presentation.

165 uses have evolved the ability to subvert MHC class I antigen presentation.

166 non-housekeeping functions required for MHC class I antigen presentation.

167 expression of multiple genes devoted to MHC class I antigen presentation.

168 rnover, and major histocompatibility complex class I antigen presentation.

169 of mechanisms, including perturbation of HLA class I antigen presentation.

170 ules associated with human leukocyte antigen class I antigen presentation.

171 arious Chlamydia species to alter direct MHC class I antigen presentation.

172 ler T cell responses by interfering with MHC class I antigen presentation.

173 dentified that inhibits TAP function and MHC class I antigen presentation.

174 pe 9 (PSMB9), both of which are required for class I antigen presentation.

175 tional protease, which are essential for MHC class I antigen presentation.

176 ic role of IFN-I and IFN-gamma in optimizing class I antigen presentation.

177 protein antigens into the APC cytoplasm for class I antigen presentation.

178 munogenicity by increasing calreticulin, MHC class I, antigen presentation and T-cell infiltration.

179 NLRC5 regulates expression of HLA class I, antigen presentation-related genes, and chemoki

180 t studies indicate a role of loss of the HLA class-I antigen presentation machinery (APM) protein bet

181 TAPBPR as an additional component of the MHC class I antigen-presentation pathway demonstrates that m

182 e with a hepatocyte-specific mutation in the class I antigen-presentation pathway, and immunopeptidom

183 igen load, but is highly correlated with MHC class I antigen presenting machinery expression (APM).

184 ells to the major histocompatibility complex class I antigen-presenting machinery.

185 residues located on the alpha-1/2 domains of class I antigen-presenting molecules primarily interface

186 s for major histocompatibility complex (MHC) class I antigens, preventing attack against healthy cell

187 lates major histocompatibility complex (MHC) class I antigen processing and presentation by inducing

188 strate that major histocompatibility complex class I antigen processing and presentation is modulated

189 Enhanced expression of the MHC class I antigen processing and presentation pathway and

190 centrosome may be an important locus for MHC class I antigen processing and that targeting antigen to

191 ated to MHC class I expression or to the MHC class I antigen processing machinery in these cells.

192 the isolated hsp molecules can enter the MHC class I antigen processing pathway of professional antig

193 ith proteasome inhibitors that block the MHC class I antigen processing pathway, but not by an inhibi

194 indings place DRiPs at the center of the MHC class I antigen processing pathway, linking immunosurvei

195 can channel bacterial proteins into the MHC class I antigen processing pathway.

196 lic delivery of peptide to the classical MHC class I antigen processing pathway.

197 endogenous major histocompatibility complex class I antigen processing pathway.

198 Consistent with its role in MHC class I antigen processing, ACE localizes to the endopla

199 e include key transitions in the cell cycle, class I antigen processing, signal transduction pathways

200 ical ubiquitination in the modulation of MHC class I antigen processing.

201 JMP syndrome, most probably by affecting MHC class I antigen processing.

202 Alterations of the MHC class I antigen-processing and presentation machinery (A

203 sms, including human leukocyte antigen (HLA) class I antigen-processing machinery (APM) defects.

204 Human leukocyte antigen (HLA) class I antigen-processing machinery (APM) plays a cruci

205 Thus, class I antigen-processing machinery can distinguish fol

206 le about the molecular basis of multiple HLA class I antigen-processing machinery defects in malignan

207 ble structural and epigenetic defects in HLA class I antigen-processing machinery in a recurrent mela

208 and tapasin, critical components of the HLA class I antigen-processing machinery, which were up-regu

209 in the ER is therefore a key step in the MHC class I antigen-processing pathway and also explains the

210 nd into the major histocompatibility complex class I antigen-processing pathway for induction of CMI

211 ility of Caki-2 cells to up-regulate the MHC class I antigen-processing pathway.

212 pression of major histocompatibility complex class I antigens, reduced demyelination, and a lengthene

213 umor-protective immunity was mediated by MHC class I antigen- restricted CD8(+) T cells together with

214 umor-protective immunity was mediated by MHC class I antigen-restricted CD8(+) T cells that secreted

215 t obtained was mediated predominantly by MHC class I antigen-restricted CD8(+) T cells with help from

216 This vaccine also induced MHC class I antigen-restricted CD8(+) T-cell responses.

217 ied to express human leukocyte antigen (HLA) class I antigen-restricted, melanoma antigen-reactive T-

218 t model (PVG.R8-to-PVG.1U) disparate for one class I antigen, RT.1Aa, we previously demonstrated that

219 h DNA encoding only membrane-bound donor MHC class I antigen (RT1.A(a)) also accelerated allograft re

220 his surprising result is that recognition of class I antigens through the direct rather than the indi

221 gulation of major histocompatibility complex class I antigen, thus preserving gut motility.

222 donor major histocompatibility complex (MHC) class I antigens to IgKO recipients.

223 4 and major histocompatibility complex (MHC) class I antigens, to alter the state of T-cell activatio

224 ong patients expressing > or = two of the M5 class I antigens, validating a prior observation in stag

225 MHC class I antigen was expressed in the three cell lines in

226 dy to major histocompatibility complex (MHC) class I antigen was highly associated with risk of reste

227 dicated that the amount of newly synthesized class I antigen was similar in uninfected and VZV-infect

228 es directed against class II but not against class I antigens was associated with a shorter duration

229 HLA immunohistochemistry for class I antigens was performed on elderly donor eyes.

230 Serological testing for HLA class I antigens was performed via microlymphocytotoxici

231 s that lack major histocompatibility complex class I antigens, we do not know what signals the attack

232 ortic allografts mismatched for a single MHC class I antigen were transplanted into athymic NUDE or R

233 Reactive class I antigens were also able to mediate deletion of m

234 Soluble class I antigens were secreted by the transfected cells

235 II homozygous cell lines that do not express class I antigens were used to study the role of the TCR

236 cells invade muscle fibres that express MHC class I antigens, which leads to fibre necrosis via the

237 pressing Ly49 inhibitory receptors for donor class I antigens, which would be predicted to have no ef