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 consistently low expression of specific HLA class I antigens.

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

8 of PKR and major histocompatibility complex class I antigens.

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

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

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

12 recipients are sensitized to mismatched HLA class I antigens.

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

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

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

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

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

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

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

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

21 antibodies identified were directed against class I antigens.

22 103 HLA class I epitopes shared by groups of class I antigens.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

56 HLA class I antigen defects are frequently found in malignan

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

75 ization and major histocompatibility complex class I antigen expression.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

96 HLA class I antigen mismatches that are serologically detect

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

192 4 and major histocompatibility complex (MHC) class I antigens, to alter the state of T-cell activatio

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

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

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

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

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

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

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

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

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

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

203 Soluble class I antigens were secreted by the transfected cells

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

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

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