ライフサイエンスコーパス: autoaggressive

1 ulitis whereas Bim-/- clone 4 cells were not autoaggressive.

2 Autoaggressive alphabeta T cells in the absence of Vgamm

3 view, we discuss how T-bet expression drives autoaggressive and inflammatory processes and how its fu

4 In the absence of T-bet, autoaggressive (anti-LCMV) CD8 lymphocytes were reduced

5 tion activating gene (RAG) 1 and RAG2 in the autoaggressive, but not in the nonautoaggressive, periph

6 portantly, numbers and effector functions of autoaggressive CD4 and CD8 lymphocytes were not decrease

7 in the CNS by preventing the development of autoaggressive CD4(+) Tregs.

8 abetes by drastically lowering activation of autoaggressive CD8 lymphocytes and their production of i

9 died whether Fas-L could protect islets from autoaggressive CD8 lymphocytes in a transgenic model of

10 30%, which was associated with a decrease of autoaggressive CD8 NP-specific lymphocytes in islets and

11 betic recipients and suppressed heterologous autoaggressive CD8 responses.

12 act that a high number of in vitro activated autoaggressive CD8 T cells can over-ride the requirement

13 we found a drastic increase in NP-specific, autoaggressive CD8 T cells in the pancreas after infecti

14 cretion of IFN-gamma-inducible protein-10 by autoaggressive CD8(+) lymphocytes might determine their

15 Identification of adhesion molecules used by autoaggressive CD8(+) T lymphocytes to enter the CNS wou

16 An autoaggressive CD8+ T cell clone can, however, transfer

17 rocessing and cross-presentation to strongly autoaggressive CTLs.

18 This facilitates its cross-presentation to autoaggressive cytotoxic MHC-E-restricted CD8(+)CD56(+)

19 because of their capacity to regulate potent autoaggressive effector cells, Treg cells partly contrib

20 LCV) are requisite APCs for MHC-E-restricted autoaggressive effector memory CTLs specific for the imm

21 ate neo-epitopes from self proteins, causing autoaggressive immune attack.

22 of CD40L blockade during development of the autoaggressive immune response completely prevented auto

23 is the initiating event in the activation of autoaggressive immune responses leading to autoimmune di

24 Autoaggressive immune-mediated illnesses secondary to gr

25 he hair follicle itself is the key target of autoaggressive immunity.

26 Recently, autoaggressive immunological responses were included amo

27 he diabetogenic potential of high numbers of autoaggressive lymphocytes through, for example, increas

28 lays an important role in the recruitment of autoaggressive lymphocytes to the islets of Langerhans.

29 d disease by interfering with trafficking of autoaggressive lymphocytes to the pancreas.

30 nd does not carry the risk for reinfusion of autoaggressive lymphocytes with the autograft.

31 on of islets of Langerhans with regenerated, autoaggressive lymphocytes.

32 system from spontaneously mounting a severe autoaggressive lymphoproliferative disease and can modul

33 s yet another soldier to the growing army of autoaggressive mechanisms that underlie RA.

34 , and this protein may act by modulating the autoaggressive phenotype that is characteristic of RASFs

35 eviation of the T-cell response away from an autoaggressive, pro-inflammatory Th1 response.

36 nes and chemokines can influence the ongoing autoaggressive process beneficially at the preclinical s

37 that allows for more precise tracking of the autoaggressive response and choice of the time point for

38 (RIP-LCMV-NP transgenic mice), in which the autoaggressive response is directed to a viral nucleopro

39 During an autoimmune process, the autoaggressive response spreads from the initiating auto

40 s evolved mechanisms to limit the risk of an autoaggressive response.

41 Identifying and quantifying autoaggressive responses in multiple sclerosis (MS) has

42 consequences of this for the development of autoaggressive responses.

43 restrain the immune system from mounting an autoaggressive systemic inflammatory response, but why t

44 iated autoimmune disease by skewing both the autoaggressive T cell and B cell responses toward a prot

45 3(+) T regulatory cells can actively control autoaggressive T cell responses.

46 ly disabling autoimmune disorder mediated by autoaggressive T cells and autoantibodies that target ce

47 s study, we report that CD40 was cloned from autoaggressive T cells and that engagement induces expre

48 inhibiting the localization and response of autoaggressive T cells in the pancreatic islets.

49 ve suggested that CD40 expression identifies autoaggressive T cells in the periphery of autoimmune pr

50 ly characterized gammadelta-TCR expressed by autoaggressive T cells in tissue.

51 tion and therefore some of these potentially autoaggressive T cells need to convert into regulatory T

52 rimental autoimmune encephalomyelitis (EAE), autoaggressive T cells traffic into the CNS and induce d

53 unity by driving activation and expansion of autoaggressive T cells via Ag presentation.

54 several regulatory T cell subsets can temper autoaggressive T cells, although it remains undetermined

55 IP), a potential mechanism for generation of autoaggressive T cells, has been poorly defined.

56 ertoire and prevents development of effector autoaggressive T cells.

57 titute a novel pathway for the generation of autoaggressive T cells.

58 minant paradigm to explain the triggering of autoaggressive T lymphocytes.

59 tation of self-antigen and the activation of autoaggressive T lymphocytes.

60 ng and release, which concomitantly prevents autoaggressive T-cell infiltration of the liver.

61 ions, the first one being the elimination of autoaggressive T-cells attacking the beta-cells, ultimat