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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

61 (1,25-(OH)(2)D(3)) is a natural inhibitor of autoimmune T cell responses in MS.

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

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

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

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

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

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

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

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

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

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

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

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

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