ライフサイエンスコーパス: autoimmune T cell

1 mediated regulation of chronically activated autoimmune T cells.

2 enic, giving rise to distinct populations of autoimmune T cells.

3 us T cells, and not by cancer cells or other autoimmune T cells.

4 expression marks a pathogenic population of autoimmune T cells.

5 te a complete lack of effect on induction of autoimmune T cells.

6 partate is an important abnormality in these autoimmune T cells.

7 T cells, we generated engineered transiently autoimmune T cells.

8 at are involved in the control of pathogenic autoimmune T cells.

9 II) to provide specificity for targeting the autoimmune T cells.

10 II) to provide specificity for targeting the autoimmune T cells.

11 s reporter transgenic to follow the onset of autoimmune T cell activation after regulatory T cell dep

12 ro with anti-CD3/anti-CD28 and IL-2 to mimic autoimmune T cell activation exhibited proliferation and

13 class II molecules and associations between autoimmune T cells and rheumatic diseases.

14 rstanding of in vivo idiotypic regulation of autoimmune T cells and the regulatory mechanism underlyi

15 pathogenic autoantibodies to DNA by causing autoimmune T-cell apoptosis, an effect that was independ

16 experimental autoimmune encephalitis (EAE), autoimmune T cells are activated in the periphery before

17 function in situ and the mechanism by which autoimmune T cells are recruited to the site of inflamma

18 pathogenesis include: 1) failure to "delete" autoimmune T cells at the level of thymic selection; 2)

19 ng bone marrow failure disorder driven by an autoimmune T cell attack against hematopoietic stem and

20 irect evidence for a p21 role in controlling autoimmune T cell autoreactivity without affecting norma

21 The mechanism by which these autoimmune T cells become activated has not been resolve

22 to T cells revealed that Fas indeed controls autoimmune T cells, but not T cells responding to strong

23 pening the early activation and migration of autoimmune T cells, but sustains the long-term progressi

24 ecretory functions; and 8) failure to remove autoimmune T cells by normal mechanisms of apoptosis.

25 eled, opportunities will emerge to interject autoimmune T cells by targeting their metabolic checkpoi

26 In type 1 diabetes, autoimmune T cells cause destruction of pancreatic beta

27 It is likely that the passage of these autoimmune T cell clones through the disrupted blood-bra

28 system cells and stimulation of the specific autoimmune T cell clones.

29 he grafts and expansion of already prevalent autoimmune T cell clonotypes residing in the endogenous

30 al that DRAK2 blockade may lead to permanent autoimmune T cell destruction via intrinsic apoptosis pa

31 mited mechanistic insight into self-reactive autoimmune T cell development and their escape from nega

32 ondria can modulate beta-cell sensitivity to autoimmune T-cell effectors.

33 y patients with inclusion body myositis, the autoimmune T cell expansion has evolved into a neoplasti

34 jor autoepitopes may reveal the mechanism of autoimmune T-cell expansion and lead to antigen-specific

35 ges in naive type II collagen (CII)-specific autoimmune T cells following a tolerogenic signal, a TCR

36 To date, no marker for autoimmune T cells has been described, although it was p

37 any one of the nucleosomal peptides impaired autoimmune T cell help, inhibiting the production of mul

38 eloping a means of therapeutically targeting autoimmune T cells in an Ag-specific manner has been dif

39 eered Tregs that have the capacity to target autoimmune T cells in an Ag-specific manner.

40 unexpected mixed phenotype of apoB-reactive autoimmune T cells in atherosclerosis and suggest an ini

41 rther our understanding of the properties of autoimmune T cells in patients with PV.

42 lity of autoimmune tissues and the rarity of autoimmune T cells in the blood hinder their study.

43 endothelial venules; 3) clonal expansion of autoimmune T cells in the glands; 4) upregulation of maj

44 We describe a method to enrich and harvest autoimmune T cells in vivo by using a biomaterial scaffo

45 nesis of IDDM involves the transmigration of autoimmune T cells into the pancreatic islets and the su

46 One way to obtain and analyze these autoimmune T cells is to alter T cell receptor (TCR) sig

47 llow molecular mimics to spuriously activate autoimmune T cells; it also underlies T cell rejection o

48 Pathogen-induced cross-activation of autoimmune T cells may occur by molecular mimicry.

49 It is accepted that autoimmune T cells mediate the early steps of new multip

50 Mounting evidence that IBM is an autoimmune T cell-mediated disease provides hope that fu

51 er, ICI can induce uncommon life-threatening autoimmune T-cell-mediated myotoxicities, including myoc

52 Psoriasis has been considered an autoimmune, T cell-mediated disorder in which adaptive i

53 spontaneous diabetes and diabetes induced by autoimmune T cells or the beta cell toxin streptozotocin

54 How autoimmune T cell populations arise and are sustained, a

55 The crystal structures of five autoimmune T cell receptor (TCR)-peptide-MHC complexes r

56 the Abs they secrete appear to modulate the autoimmune T cell repertoire by down-regulating T cell e

57 Together, these results show that the autoimmune T cell repertoire is influenced by the concom

58 f thymic selection for the generation of the autoimmune T cell repertoire.

59 In this study, we examined the autoimmune T cell response in bullous pemphigoid patient

60 ath of the CNS thought to be targeted by the autoimmune T cell response in multiple sclerosis (MS).

61 These studies suggest that the autoimmune T cell response in the islets may be temporar

62 allogeneic B10.A (H2a) splenocytes led to an autoimmune T cell response toward the dominant self-pept

63 diol treatment altered the Th profile of the autoimmune T cell response, which, in turn, altered the

64 nal APCs may then amplify and perpetuate the autoimmune T cell response.

65 a unique means to controlling the polyclonal autoimmune T cell response.

66 To dissect the autoimmune T-cell response against human beta-cells, we

67 lts from the destruction of beta-cells by an autoimmune T-cell response assisted by antigen-presentin

68 urpose of this study was to characterize the autoimmune T-cell response associated with FS.

69 t cardiac transplantation in mice induces an autoimmune T-cell response to a heart tissue-specific pr

70 development and/or maintain Th2 bias against autoimmune T cell responses against new B cell Ag recept

71 Moreover, ASCs suppressed autoimmune T cell responses and increased the percentage

72 bute to disease induction, but instead limit autoimmune T cell responses and prevent multiple-scleros

73 are required as APCs to generate pathogenic autoimmune T cell responses and provide a direct correla

74 important role in regulating both normal and autoimmune T cell responses by exerting a direct effect

75 a suggest the potential for interfering with autoimmune T cell responses by inhibition of Jak3 signal

76 (1,25-(OH)(2)D(3)) is a natural inhibitor of autoimmune T cell responses in MS.

77 e cells with a distinct capacity to regulate autoimmune T cell responses that differs from that used

78 ng cause of blindness and thought to involve autoimmune T cell responses to retinal proteins (e.g., r

79 inhibition of PKCtheta is expected to block autoimmune T cell responses without compromising antivir

80 to tumors and viruses, while suppressing CD4 autoimmune T cell responses.

81 en processing, leading to the development of autoimmune T cell responses.

82 e role of B cells as auto-APCs in activating autoimmune T cells responses.

83 Peripheral antiviral and autoimmune T-cell responses were normal, and disease sev

84 d, and the molecular programmes defining the autoimmune T cell state, are unknown.

85 The primary driver of type I diabetes is the autoimmune T cells that destroy insulin-producing beta-c

86 atment, the immune system's involvement with autoimmune T cells that recognize the protein alpha-synu

87 nd the development of therapeutics targeting autoimmune T cells, their cognate antigens, or their und

88 n is prone to escape of initially controlled autoimmune T cells through cross reactivity to pathogens

89 sticity; thirdly, the possible resistance of autoimmune T cells to T(reg)-mediated control; and fourt

90 -associated APCs provides stimuli that guide autoimmune T cells to the CNS destination, enabling them

91 investigate the migration and specificity of autoimmune T cells to the inflammatory site, we used the

92 immunity by shifting the cytokine profile of autoimmune T cells toward a protective T helper 2 cell (

93 that T(reg) cells and potentially pathogenic autoimmune T cells use overlapping pools of self-reactiv

94 esults toward a unified understanding of the autoimmune T cell: which genes, cell states, and antigen