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 he intestinal surface, and protected against Listeria monocytogenes infection.

3 or inflammasome induction to protect against Listeria monocytogenes infection.

4 and conferred protection against recombinant Listeria monocytogenes infection.

5 and dampened innate immune responses against Listeria monocytogenes infection.

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

7 -lived effector cells in vivo in response to Listeria monocytogenes infection.

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

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

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

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

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

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

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

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

16 ntaneous immune activation and resistance to Listeria monocytogenes infection.

17 LXRalpha nuclear receptor to defend against Listeria monocytogenes infection.

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

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

20 domonas aeruginosa pneumonia or disseminated Listeria monocytogenes infection.

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

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

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

24 priming but, paradoxically, promote splenic Listeria monocytogenes infection.

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

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

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

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

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

30 lymphoid and tertiary tissues following oral Listeria monocytogenes infection.

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

32 so strongly lymphocyte dependent operates in Listeria monocytogenes infection.

33 istence in mice following LCMV Armstrong and Listeria monocytogenes infection.

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

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

36 uring lymphocytic choriomeningitis virus and Listeria monocytogenes infections.

37 show that heterogeneity in susceptibility to Listeria monocytogenes infection among primary human vas

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

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

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

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

42 ate that VPA increases the susceptibility to Listeria monocytogenes infection and suggest that NK cel

43 ixture enhances both host resistance against Listeria monocytogenes infection and the therapeutic eff

44 leading to impaired T cell responses against Listeria monocytogenes infection and tumor growth.

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

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

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

48 Using LISTERIA: monocytogenes infection as an infectious disea

49 P2X5 is a protective immune regulator during Listeria monocytogenes infection, as P2X5-deficient mice

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

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

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

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

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

55 nous in vivo ISGylome in the liver following Listeria monocytogenes infection by combining murine mod

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

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

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

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

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

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

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

63 To dissect how Listeria monocytogenes infection elicits NK cell activat

64 Listeria monocytogenes infection generates major histoco

65 Listeria monocytogenes infection generates T helper 1 (T

66 tion and profilin (PRF) confer resistance to Listeria monocytogenes infection in a CCR2-dependent man

67 virus infection in ACAT-deficient cells, and Listeria monocytogenes infection in ACAT-deficient cells

68 8(+) T cells that provide protection against Listeria monocytogenes infection in an Ag-specific fashi

69 at were efficacious against tumor growth and Listeria monocytogenes infection in an antigen-specific

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

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

72 2 degrees) memory CD8 T cell pool induced by Listeria monocytogenes infection in mice.

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

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

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

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

77 cell activation in vitro and in response to Listeria monocytogenes infection in vivo.

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

79 he regulation of the early innate control of Listeria monocytogenes infection in vivo.

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

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

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

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

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

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

86 Lastly, using a mouse Listeria monocytogenes infection model, we demonstrate t

87 Listeria monocytogenes infection of endothelial cells up

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

89 and resident memory T cells after foodborne Listeria monocytogenes infection of mice.

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

91 mice show an inability to control sublethal Listeria monocytogenes infection, reduced immune cell fu

92 2(-/-) mice are markedly more susceptible to Listeria monocytogenes infection than are wild-type mice

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

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

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

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

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

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

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

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

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

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

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

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

105 Macrophages activated during Listeria monocytogenes infection were more susceptible t

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