ライフサイエンスコーパス: Tc1 cell

1 L-10, a critical chemokine for attraction of Tc1 cells.

2 omoting the generation of VLA-4(+) antitumor Tc1 cells.

3 terfering RNA-mediated silencing of CD49d on Tc1 cells.

4 ototypical stimulator of IFN-gamma-producing Tc1 cells.

5 greater numbers in the tumor than deficient Tc1 cells.

6 inflammatory conditions mediated by Th1 and Tc1 cells.

7 e role of selectins using in vitro-generated Tc1 cells.

8 oted proliferative rates and invasiveness of TC1 cells.

9 tal factor for the differentiation of Th1 or Tc1 cells.

10 ype (CD127(hi)/KLRG-1(low)) as compared with Tc1 cells.

11 imarily mediated by CD8+ T cytotoxic type I (Tc1) cells.

12 However, wild-type Tc1 cells accumulate to significantly greater numbers in

13 Donor Tc1 cells administered 7 days posttumor challenge locali

14 mma interferon (IFN-gamma)-producing Th1 and Tc1 cells after inoculation of live virus occurred indep

15 expression of VLA-4 on Tc1 versus Tc2 cells, Tc1 cells alone were competent to adhere to plate-bound

16 r in T helper 1 (Th1) and effector CD8(+) T (Tc1) cells, although T-bet was dispensable in CD8 effect

17 CD8+ IL-17-producing cells are distinct from Tc1 cells and are important in effector functions at the

18 ng of adoptive-transferred, antigen-specific Tc1 cells and suggest that more effective vaccine and/or

19 rocess of allograft rejection: IFN-gammahigh Tc1 cells are important in early graft vasculitis, altho

20 show that adoptively transferred Ag-specific Tc1 cells are more effective in delaying mammary tumor g

21 ty through distinct effector mechanisms, but Tc1 cells are superior to Tc17 cells in mediating tumor

22 in, and the role of CD8+ type 1 cytotoxic T (Tc1) cells as effector cells has been demonstrated.

23 xpressed by subsets of Th1 or T-cytotoxic 1 (Tc1) cells, but not by Th2 or Tc2 cells, establishing Bo

24 Almost all Bonzo+ Tc1 cells contain preformed granzyme A and display cytot

25 This suggests that CD8+ Tc1 cells could play a pathogenic role in central nervou

26 SE-labeled wild-type and IFN-gamma-deficient Tc1 cells divide rapidly in secondary lymphoid organs, i

27 ribute to the development of pathogenic Th1 (Tc1) cells during the diabetogenic response.

28 S administration reduced CD4(+)Th1 and CD8(+)Tc1 cell expansion to alloantigen and, in a separate mod

29 Proliferative rates of melanoma (B16F10) and TC1 cells exposed to IH either in single culture or in c

30 Tc1 cells from mice lacking IFN-gamma, however, control

31 st cells to the draining lymph node, whereas Tc1 cells from perforin-deficient donors are unimpaired.

32 nhanced the tumor-homing of i.v. transferred Tc1 cells in a CXCL-10-dependent fashion.

33 the growth of established melanoma, whereas Tc1 cells induced long-term tumor regression.

34 Finally, the efficient trafficking of Tc1 cells into intracranial M05 lesions in vivo was effi

35 P- and E-selectin-independent migration of Tc1 cells into the inflamed skin was predominantly media

36 igh IL-5high Tc2, but not of IL-4low IL-5low Tc1 cells lead to extensive infiltration of eosinophils

37 17 and IFNgamma-producing CD8(+) T (Tc17 and Tc1) cells, likely via suppression of lactate-driven PD-

38 After ACT, Tc1 cells maintained their phenotype to produce IFN-gamm

39 Mechanistically, Tc1 cells mediated antitumor immunity primarily through

40 y P- and E-selectin, as shown by the reduced Tc1 cell migration into the inflamed skin of mice defici

41 ndicate that all three selectins can mediate Tc1 cell migration into the inflamed skin.

42 ed stimulation of CD8(+) T cells to generate Tc1 cells, not only increases IFNgamma production but al

43 not consistently observed in mice receiving Tc1 cells or unmanipulated CD8 cells.

44 Except of CLA(-) Tc1 cells (P = .03), IFN-gamma levels were mostly simila

45 ring P- and E-selectin-mediated migration of Tc1 cells, P-selectin glycoprotein ligand-1 appears to b

46 Tc1 cells persisted, whereas Tc2 cell numbers progressiv

47 While Tc1 cells produced IFN-gamma and efficiently killed targ

48 primary T cells redirects them into Th1 and Tc1 cells, respectively, as evidenced by the simultaneou

49 or T2 conditions indeed generated murine TH1/TC1 cells secreting interleukin-2/interferon-gamma (IL-2

50 lso accumulated to a greater extent than did Tc1 cells, suggesting that adoptive transfer of CD8 T ce

51 Compared with type-I CD8(+) cytotoxic T (Tc1) cells, Tc9 secreted different cytokines and were le

52 expressed at significantly higher levels on Tc1 cells than on Tc2 cells.

53 Conversely, Tc1 cell transfer markedly delayed the appearance of cor

54 poptosis as compared with IFN-gamma knockout Tc1 cell-treated hosts.

55 Lung epithelial TC1 cell tumors were 84% greater in mice subjected to IH

56 After viral challenge, Tc1 cells underwent more efficient expansion than did Tc

57 -gamma secreted by donor cytotoxic T cell 1 (Tc1) cells was the most important factor in promoting EG

58 cient expansion than did Tc2 cells, and only Tc1 cells were detected at the site of infection.

59 nt increase in IFN-gamma-secreting activity (Tc1 cells), were responsible for the tumor protection.

60 cells, and 60-65% of Bonzo+ CD8 T cells are Tc1 cells, while few Bonzo+ cells are type 2 T cells.