ライフサイエンスコーパス: Listeria monocytogenes infection

1 uced tolerance and more effective control of Listeria monocytogenes infection.

2 and conferred protection against recombinant Listeria monocytogenes infection.

3 cing CD4(+) and CD8(+) T cells responding to Listeria monocytogenes infection.

4 tion of memory CD8(+) T cells in response to Listeria monocytogenes infection.

5 Tim-3 affects CD8 T cell responses to acute Listeria monocytogenes infection.

6 survival of CD8(+) T cells in vivo following Listeria monocytogenes infection.

7 n the innate immune response of mice against Listeria monocytogenes infection.

8 increased bacterial burden in the liver upon Listeria monocytogenes infection.

9 ive secondary, but not primary, responses to Listeria monocytogenes infection.

10 ector CD8+ T cell populations in response to Listeria monocytogenes infection.

11 and dampened innate immune responses against Listeria monocytogenes infection.

12 LXRalpha nuclear receptor to defend against Listeria monocytogenes infection.

13 mly express high levels of alpha4beta7 after Listeria monocytogenes infection.

14 huS4 strain and in a mouse model of systemic Listeria monocytogenes infection.

15 domonas aeruginosa pneumonia or disseminated Listeria monocytogenes infection.

16 ophils in the spleen than did WT mice during Listeria monocytogenes infection.

17 r for Listeria adhesion protein (LAP) during Listeria monocytogenes infection.

18 tion and an enhanced immune response against Listeria monocytogenes infection.

19 on of Ag-specific CD8 T cells in response to Listeria monocytogenes infection.

20 primary and memory CD8(+) T cell response to Listeria monocytogenes infection.

21 mpaired CD8(+) T cell expansion in vivo upon Listeria monocytogenes infection.

22 nd/or sustaining CD8 T cell memory following Listeria monocytogenes infection.

23 s develop a normal CD8(+) T cell response to Listeria monocytogenes infection.

24 an impaired T helper type 1 response during Listeria monocytogenes infection.

25 lymphoid and tertiary tissues following oral Listeria monocytogenes infection.

26 rom primary effector to memory T cells after Listeria monocytogenes infection.

27 so strongly lymphocyte dependent operates in Listeria monocytogenes infection.

28 formation in response to vaccinia virus and Listeria monocytogenes infections.

29 ccinia virus, vesicular stomatitis virus, or Listeria monocytogenes infections.

30 uring lymphocytic choriomeningitis virus and Listeria monocytogenes infections.

31 MHC class II-specific GC-Tfh cells following Listeria monocytogenes infection and a 2-fold decrease f

32 e generated fewer IL-10+ T cells during both Listeria monocytogenes infection and experimental autoim

33 eractions required for resistance to primary Listeria monocytogenes infection and have illustrated th

34 defensive role of the gut microbiota against Listeria monocytogenes infection and identify intestinal

35 colony-stimulating factor (G-CSF), CXCL2, or Listeria monocytogenes infection are absent or impaired,

36 ry and memory CD8 T cell responses following Listeria monocytogenes infection are enhanced by the abs

37 PGRN-deficient mice failed to clear Listeria monocytogenes infection as quickly as WT and al

38 Using LISTERIA: monocytogenes infection as an infectious disea

39 sponse to P. aeruginosa, S. typhimurium, and Listeria monocytogenes infection, as well as in response

40 hat CCR2 deficiency markedly worsens hepatic Listeria monocytogenes infection because Ly6C(high) mono

41 s Ib molecules expand rapidly during primary Listeria monocytogenes infection but only minimally upon

42 T cell response and are more susceptible to Listeria monocytogenes infection, but have substantially

43 t expansion of CD8(+) T cell response during Listeria monocytogenes infection, but plays a key role i

44 trated that the innate resistance of mice to Listeria monocytogenes infection by intravenous or intra

45 T-bet (DKO) could not be rescued from lethal Listeria monocytogenes infection by prior treatment with

46 ella tularensis live vaccine strain (LVS) or Listeria monocytogenes infection can be stimulated eithe

47 ng in vivo memory CD8(+) T-cell responses to Listeria monocytogenes infection, CTLA-4 blockade enhanc

48 Upon acute Listeria monocytogenes infection, deleting miR-23a in T

49 Recent analyses of CD8 T cell responses to Listeria monocytogenes infection demonstrate that the du

50 cytes are more resistant than normal mice to Listeria monocytogenes infection during the early innate

51 To dissect how Listeria monocytogenes infection elicits NK cell activat

52 Listeria monocytogenes infection generates major histoco

53 Listeria monocytogenes infection generates T helper 1 (T

54 8(+) T cells that provide protection against Listeria monocytogenes infection in an Ag-specific fashi

55 tegrins, we examined CD8 T cell responses to Listeria monocytogenes infection in CD11a-, CD11b-, and

56 (+) T cell formation and their function upon Listeria monocytogenes infection in mice.

57 2 degrees) memory CD8 T cell pool induced by Listeria monocytogenes infection in mice.

58 cells conferred increased protection against Listeria monocytogenes infection in susceptible IFN-gamm

59 a T cells are important for the clearance of Listeria monocytogenes infection in the intestinal mucos

60 y impaired effector T cell development after Listeria monocytogenes infection in vivo and c-FLIP(L)-d

61 are more susceptible to endotoxic shock and Listeria monocytogenes infection in vivo, possibly due t

62 ticulate antigen in vitro and to recombinant Listeria monocytogenes infection in vivo.

63 LT have been uncovered: as a host factor for Listeria monocytogenes infection, in the maintenance of

64 tantly, VM cells showed efficient control of Listeria monocytogenes infection, indicating memory-like

65 ere we show that antibiotic treatment before Listeria monocytogenes infection induced numbers of prot

66 In this report we demonstrate that Listeria monocytogenes infection induces distinct CD8(+)

67 ate that fetal wastage triggered by prenatal Listeria monocytogenes infection is driven by placental

68 ainst microbial infections, we have used the Listeria monocytogenes infection model to explore the im

69 Listeria monocytogenes infection of endothelial cells up

70 The role of sigma(B) in Listeria monocytogenes infection of human intestinal epi

71 f cardiac transplantation, we show that when Listeria monocytogenes infection precipitates acute reje

72 2(-/-) mice are markedly more susceptible to Listeria monocytogenes infection than are wild-type mice

73 cted T cells respond more rapidly to primary Listeria monocytogenes infection than conventional MHC c

74 l uptake and were more susceptible to lethal Listeria monocytogenes infection than were DT-treated CL

75 CD8(+) T cell responses to Listeria monocytogenes infection that are restricted by

76 tal numbers of Ag-specific CD8 T cells after Listeria monocytogenes infection that were similar to th

77 ough IFN-gamma is required for resolution of Listeria monocytogenes infection, the identities of the

78 tion of B cells at different times following Listeria monocytogenes infection to show that B cells ar

79 immunosuppression, because susceptibility to Listeria monocytogenes infection was not altered.

80 We show that CD8(+) T cell expansion after Listeria monocytogenes infection was primarily dependent

81 , a chemokine that is induced by IL-4 during Listeria monocytogenes infection, was detected at betwee

82 By carefully modulating the kinetics of Listeria monocytogenes infection, we analyzed the requir

83 tion were lymph node dependent, responses to Listeria monocytogenes infection were driven primarily i

84 ns of the alternative sigma factor sigmaB to Listeria monocytogenes infection were investigated using

85 Macrophages activated during Listeria monocytogenes infection were more susceptible t

86 infection differed significantly than during Listeria monocytogenes infection with a substantial redu