ライフサイエンスコーパス: class II antigen

1 T cells or major histocompatibility complex class II antigen.

2 EPC, neonatal knockout EPC expressed little class II antigen.

3 elial expression of major histocompatibility class II antigens.

4 ed by the complete lack of expression of MHC class II antigens.

5 peptides in the context of both class I and class II antigens.

6 orst when the donor and recipient shared MHC class II antigens.

7 nts can develop anti-HLA antibodies to donor class II antigens.

8 essed major histocompatibility complex (MHC) class II antigens.

9 ree cases, antibodies were against donor HLA class II antigens.

10 are being activated by mismatched donor HLA-class II antigens.

11 All aspirates were negative for MHC class II antigens.

12 cted at major histocompatibility class (MHC) class II antigens.

13 d expression of FCgammaRI, CR3, CR4, and MHC class II antigens.

14 I and major histocompatibility complex (MHC) class II antigens.

15 heat shock cognate 70; histocompatibility 2, class II antigen A, alpha; and the T cell cytokine recep

16 0), and DQ8.Ab(0), lacking their own (mouse) class II antigens (Ab(0)), on the original (arthritis-re

17 ass II(-) but that are capable of expressing class II antigen after surgery and migrating to draining

18 nt in major histocompatibility complex (MHC) class II antigen (Ag)-T-cell receptor (TCR), B7-CD28, or

19 cell major histocompatibility complex (MHC) class II antigen and for gamma-interferon (gamma-IFN), i

20 he minimal truncated form that binds the MHC Class II antigen and triggers superoxide production thro

21 s in the cell surface expression of both MHC class II antigens and IL-4 receptor are completely abrog

22 Intestinal epithelial cells can express HLA class II antigens and may function as antigen-presenting

23 nalysis demonstrated eight were specific for class II antigens and one for class I antigens.

24 nizing donor antigens presented by recipient class II antigens, and (2) CD8+ cells can participate as

25 ce lacking the cytoplasmic tail of their MHC class II antigens, and mice depleted of CD4+ cells by an

26 nt; almost all de novo DSAs were against HLA class II antigens, and the majority were against DQ anti

27 phase matrix to which soluble HLA class I or class II antigens are attached is significantly more sen

28 se of the disease since both HLA class I and class II antigens are critical to the interaction betwee

29 Thus, MHC class II antigens are essential for the expression of au

30 major histocompatibility complex class I and class II antigens as well as the costimulatory molecules

31 h expressed major histocompatibility complex class II antigen; B cells and exogenous monocytes/macrop

32 ndosomes/lysosomes, possibly after or before class II antigen binding.

33 l hydrogen bonds at the opposite ends of the class II antigen-binding groove (beta-His-81, beta-Asn-8

34 of peptide residues projecting from the MHC class II antigen-binding groove as part of a mini beta s

35 on of the Ii-derived (CLIP) peptide from the class II antigen-binding pocket and subsequent peptide l

36 and canine major histocompatibility complex class II antigens but is reactive with a narrower spectr

37 ng of major histocompatibility complex (MHC) class II antigens by anti-HLA-DR monoclonal antibody (Mo

38 onor class II antigens or modified recipient class II antigens; (c) isotype switching from IgM to IgG

39 esses major histocompatibility complex (MHC) class II antigens constitutively.

40 In previous studies, absence of donor MHC class II antigens did not affect skin graft survival, bu

41 Absence of donor MHC class II antigens did not affect the production of eithe

42 rminants, CD138 and major histocompatibility class II antigens, distinguish developing B-1 cells from

43 patients, with the majority directed at HLA class II antigens (DR, 41%; DQ, 53%).

44 nduced pulmonary fibrosis and identified MHC class II antigen Ealpha (H2-Ea) as a risk factor for thi

45 ein (GFAP) and (3) staining for OX-6, an MHC class II antigen expressed by microglia and macrophages.

46 from horses with uveitis had clusters of MHC class II antigen-expressing cells, T lymphocytes, and en

47 s of scid mice with evidence of enhanced MHC class II antigen expression and increased phagocytosis (

48 his study determines the effect of E2 on MHC class II antigen expression in the allograft, in the abs

49 associated with inhibition of inducible MHC class II antigen expression in the allografts.

50 estradiol-17beta abolition of inducible MHC class II antigen expression in the aorta allograft occur

51 f cardiac allograft recipients abolishes MHC class II antigen expression in the coronary arteries and

52 E2 treatment, we observed that inducible MHC class II antigen expression is abolished in the media of

53 We have observed high constitutive levels of class II antigen expression on porcine and human coronar

54 by 2-5 d; the associated upregulation of MHC class II antigen expression suggested increased immunoge

55 gulation of major histocompatibility complex class II antigen expression was also noted.

56 MHC class II antigen expression was not detectable in allogr

57 (H&E, collagen) and immunohistochemical (MHC class II antigen expression, infiltration of T and B lym

58 on of major histocompatibility complex (MHC) class II antigen expression, T lymphocytes, and macropha

59 gulation of major histocompatibility complex class II antigen expression.

60 gans associated with the upregulation of MHC class II antigen expression.

61 genic C57BL/6 mouse strains differing in MHC class II antigen expression.

62 essed major histocompatibility complex (MHC) class II antigens for at least 48 h in vitro.

63 oid A family, three major histocompatibility class II antigen genes, and various cytokine-related gen

64 pression of major histocompatibility complex class II antigens (>75%), interleukin (IL) 2 receptor (5

65 These studies indicate that the MHC class II antigen haplotype controls myocarditis suscepti

66 and nonclassical HLA class I as well as HLA class II antigens have been identified in malignant lesi

67 taining the major histocompatibility complex class II antigen, HLA-DR.

68 Absence of recipient MHC class II antigens, however, led to production of only Ig

69 the murine major histocompatibility complex class II antigen I-Ak expressed on M12.C3.F6 cells has 1

70 Th2 (IL-4+) cell response, express both MHC class II antigens (IA(d), IE(d)) and are atherosclerosis

71 r levels of major histocompatibility complex class II antigens (IEk) than spleen DCs.

72 pecific for major histocompatibility complex class II antigens) immunolabeling and Arc fluorescence i

73 SLA class I and the induction of SLA class II antigen in response to interferon-gamma treatme

74 e of rodent species, express basal levels of class II antigens in a manner similar to that observed i

75 show that the effector T cells recognize MHC class II antigens in association with a peptide from the

76 pression of major histocompatibility complex class II antigens in F4/80(+) and CD11b+ spleen cells.

77 The role of major histocompatibility complex class II antigens in hematopoiesis is not well defined.

78 To further explore the role of MHC class II antigens in kidney graft rejection, we performe

79 s and suggest that the additional absence of class II antigens in TGF-beta1(-/-);MHC-II(-/-) mice may

80 ecules, and major histocompatibility complex class II antigens in the engrafted organ.

81 These results support a role of MHC class II antigens in the kidney regulating immune cells

82 Upregulation of major histocompatibility class II antigens increased organ immunogenicity.

83 renal allograft rejection, expression of MHC class II antigens is up-regulated on the parenchymal cel

84 ells, and the Abs tested were antimature MHC class II antigen (lacking the invariant chain) and anti-

85 the cytoplasmic tail of the recipient's MHC class II antigens led to the production of slightly redu

86 also were located in the compartment for MHC class II antigen loading (MIIC).

87 Second, they show features of MHC class II antigen-loading competent compartments for cath

88 al markers (major histocompatibility complex class II antigen, macrophage, and CD4- and CD8-positive

89 and for immunohistochemical staining of MHC class II antigens, macrophages, CD4 and CD8 T lymphocyte

90 Overall, class II antigen mismatches were associated with more re

91 the mean number of mismatches for Class I or Class II antigens, nor could any Class I/II phenotype fo

92 xpression of costimulatory molecules and MHC class II antigen on DCs isolated from livers of FL-treat

93 antibodies against allogeneic MHC class I or class II antigens on the development of early high-grade

94 histocompatibility complex (MHC) class I and class II antigens on their surface and to interact with

95 l CD4+ cell population (due to expression of class II antigens only on thymic epithelium), mice lacki

96 r histocompatibility complex class I but not class II antigens or B7 costimulatory molecules.

97 rom CD4+ cells, which recognize either donor class II antigens or modified recipient class II antigen

98 ance of antibodies directed against some HLA class II antigens, particularly HLA-DP, is less clear wi

99 The possibility that MIF participates in class II antigen presentation and/or as a chaperone is d

100 s expression of the major histocompatibility class II antigen presentation apparatus, via secreted IL

101 y classical major histocompatibility complex class II antigen presentation but also nonclassical CD1d

102 In addition to showing deficient MHC class II antigen presentation in a subset of HRS cells,

103 Recent progress in the study of class II antigen presentation includes the identificatio

104 on of major histocompatibility complex (MHC) class II antigen presentation is believed to be among th

105 Induction of the MHC class II antigen presentation machinery by cotransfectin

106 adation of two essential proteins in the MHC class II antigen presentation pathway: HLA-DR-alpha and

107 histocompatibility complex (MHC) class I and class II antigen presentation pathways, functioning in c

108 he increased efficacy of MHC class I and MHC class II antigen presentation relative to a control scFv

109 ed markedly differing dependence on host MHC class II antigen presentation, depending on the donor sp

110 of ICP34.5 in precluding autophagy-mediated class II antigen presentation, thereby enhancing the vir

111 regulatory module that programs enhanced MHC class II antigen presentation.

112 skewing, T cell receptor signaling, and MHC class II antigen presentation.

113 in in vivo to improved DC activation and MHC class II antigen presentation.

114 w of the ins and outs of MHC class I and MHC class II antigen presentation.

115 may disrupt major histocompatibility complex class II antigen presentation.

116 intracellular degradation pathway, regulates class II antigen presentation.

117 nced activity of the classic MHC class I and class II antigen-presentation pathways.

118 ressing the major histocompatibility complex class II antigen-presenting cell function of macrophages

119 ophages and major histocompatibility complex class II antigen-presenting cells in the bone resorption

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

121 rotein that impairs both the MHC class I and class II antigen-presenting pathways.

122 at line the peptide-binding pockets of HLA's Class II antigen-presenting proteins is superimposed on

123 ead, recall Th1 response was elicited by MHC class II(+) antigen-presenting cells at the site of infe

124 ed by other major histocompatibility complex class II(+) antigen-presenting cells.

125 s observed in these chimeras, as long as rat class II+ antigen-presenting cells remain in their thymi

126 iant chain (Ii) plays a critical role in MHC class II antigen processing by stabilizing peptide-free

127 ge of major histocompatibility complex (MHC) class II antigen processing enzymes in order to evade or

128 gest the use of two distinct pathways of HLA class II antigen processing in enterocytes with differen

129 h the major histocompatibility complex (MHC) class II antigen processing pathway can be recognized by

130 ined through a molecular analysis of the HLA class II antigen processing pathway.

131 In an attempt to enhance MHC class II antigen processing, we linked the sorting signa

132 but not by an inhibitor (chloroquine) of MHC class II antigen processing.

133 plex class II molecule, HLA-DO, inhibits the class II antigen-processing pathway.

134 Further, effector pathways triggered by class II antigens promote renal injury during rejection.

135 red to collectively as IDDM1), including the class II antigen receptor genes, which control the major

136 restricted CD8(+) T cells with help from MHC class II antigen-restricted CD4(+) T lymphocytes.

137 ds coated with human leukocyte antigen (HLA) class II antigens showed no class II antibodies in sera

138 on of major histocompatibility complex (MHC) class II antigen-specific CD4(+) T cell responses in DCs

139 Although activated human T cells express MHC class II antigens, the regulation of these antigens in T

140 y trigger an autoimmune reaction against MHC class II antigens through mimicry.

141 an adult pattern, but failed to up-regulate class II antigen to the high level seen among cultured a

142 enase interacts with diabetes-associated MHC class II antigens to limit T-cell activation.

143 The contribution of MHC class II antigens to the genesis of this phenotype has b

144 order, but without narcolepsy, underwent HLA class II antigen typing: 84% (N=21) were DQwl (DQB1*05,0

145 mice whose major histocompatibility complex class II antigen was replaced with the human leukocyte a

146 with enhanced expression of HLA class I and class II antigens was detected in FP-cultured DCs as com

147 Antibodies against 96 class I and 76 class II antigens were investigated and patients had a m

148 Antibodies to donor class II antigens were slightly more common, occurring i

149 vagina, but major histocompatibility complex class II antigens were still partially upregulated in th

150 red mice that did not express MHC class I or class II antigens were used to study the allorecognition

151 presses increased amounts of MHC class I and class II antigens when transplanted to SCID mice.