ライフサイエンスコーパス: carditis

1 ion with the spirochete results in increased carditis.

2 rial burdens in the heart and increased Lyme carditis.

3 he accumulation of leukocytes in murine Lyme carditis.

4 nd followed the development of arthritis and carditis.

5 s in the heart, including the development of carditis.

6 i can result in development of arthritis and carditis.

7 ot abrogate development of Lyme arthritis or carditis.

8 r, it resulted in increased severity of Lyme carditis.

9 ole in the development of Lyme arthritis and carditis.

10 sis, and Sir David Dundas on acute rheumatic carditis.

11 th B cells and T cells but have no effect on carditis.

12 the subsequent development of arthritis and carditis.

13 cterial thrombotic endocarditis or infective carditis.

14 not CD11b-/- mice, developed aggravated Lyme carditis after exposure to B. burgdorferi.

15 to cardiac myosin were similar in rheumatic carditis among a small sample of worldwide populations,

16 cells can promote resolution of murine Lyme carditis and are the first demonstration of a beneficial

17 Antisera to Arp or DbpA induced both carditis and arthritis remission but did not significant

18 Carditis and arthritis was determined by blinded histopa

19 age ankle diameter and histologic scores for carditis and arthritis were significantly higher after 2

20 ve T cells and B cells induced resolution of carditis and arthritis, 3) infected mice reconstituted w

21 elia burgdorferi results in the remission of carditis and arthritis, as well as global reduction of s

22 Infected MyD88(-/-) mice developed carditis and arthritis, similar to the disease in wild-t

23 culation, immunocompetent mice resolved both carditis and arthritis, whereas foci of myocarditis and

24 matory infiltrates during Lyme arthritis and carditis and demonstrate the coexistence of multiple mac

25 the evidence basis for defining subclinical carditis and including it as a major criterion of the Jo

26 nflammatory heart diseases such as rheumatic carditis and myocarditis.

27 be critical for resolution of arthritis and carditis and that protective antibodies are generated du

28 pressed at the lesional level in murine Lyme carditis and to demonstrate a Th1 pattern of cytokine ex

29 cted course of arthritis, a low incidence of carditis, and absence of other major manifestations of a

30 The findings of cardiac mucosa, carditis, and intestinal metaplasia in an endoscopically

31 blood lymphocytes of patients with rheumatic carditis, and mAb 10.2.5, produced from a tonsil, were c

32 to test the hypothesis that cardiac mucosa, carditis, and specialized intestinal metaplasia at an en

33 for C3H mice but did not cause arthritis or carditis, and spirochetes were at low levels or absent i

34 Anemia, thrombocytopenia, hepatitis, carditis, and splenomegaly were noted in all mice during

35 The development of arthritis and carditis, and the resolution of arthritis, were similar

36 Development of Lyme carditis appeared to be independent of modulation by IL-

37 Doppler echocardiography in the diagnosis of carditis as a major manifestation of acute rheumatic fev

38 alysis revealed no change in the severity of carditis between wild-type and IFNgamma-deficient mice a

39 rate ameliorates the severity of murine Lyme carditis by at least two mechanisms.

40 position of inflammatory infiltrates in Lyme carditis by promoting the accumulation of leukocytes ass

41 that cross-reactive antibodies in rheumatic carditis cause injury at the endothelium and underlying

42 Fatal Lyme carditis caused by the spirochete Borrelia burgdorferi r

43 yosin, there is no unifying hypothesis about carditis caused globally by many different serotypes.

44 beta2 integrin chain develop aggravated Lyme carditis, compared to that developed by wild-type (WT) m

45 ned disease conditions such as arthritis and carditis differed in severity in mice infected solely wi

46 ntrolling the development of aggravated Lyme carditis, disease induction was analyzed in CD11a-/-, CD

47 inflammation in cardiac epithelium (gastric carditis) have yielded contradictory results, perhaps be

48 ercent, aseptic meningitis in 2 percent, and carditis in 0.5 percent.

49 An analysis of rheumatic carditis in a Pacific Islander family confirmed the pres

50 ut was no longer able to cause arthritis and carditis in C3H mice.

51 suggest that the increased severity of Lyme carditis in CD18 hypomorph mice is caused by deficiency

52 rdiac myosin in the development of rheumatic carditis in humans.

53 s hypothesis, we examined the course of Lyme carditis in mice selectively deficient in B cells or alp

54 Arthritis and carditis in mice that had immunizing infections with B.

55 t may be important in the resolution of Lyme carditis in mice.

56 R2 on the development and resolution of Lyme carditis in resistant (C57BL/6J [B6]) and sensitive (C3H

57 he development and severity of arthritis and carditis in the C3H IL-17RA(-/-) mice were similar to wh

58 he controversy regarding the role of gastric carditis in the development of metaplasia and neoplasia

59 degree conduction block associated with Lyme carditis in the United States.

60 The enhancement of Lyme carditis in these mice is characterized by increased mac

61 Lyme carditis is an uncommon manifestation of Lyme disease th

62 The cardiac infiltrate seen in murine Lyme carditis is composed predominantly of macrophages, but s

63 hird-degree heart block associated with Lyme carditis is essential to providing prompt and appropriat

64 can be recurrent or prolonged, whereas Lyme carditis is mostly nonrecurring.

65 A prominent difference between arthritis and carditis is the differential representation of phagocyte

66 PSReA have been reported to have late onset carditis, it is judicious to recommend that patients wit

67 he pathogenic antibody response in rheumatic carditis may reflect the conversion of a T-cell-independ

68 ease in certain hosts, such as arthritis and carditis, may be autoimmunity mediated due to molecular

69 e sudden cardiac deaths associated with Lyme carditis occurred from late summer to fall, ages ranged

70 s resolution without affecting the status of carditis or influencing the status of infection, includi

71 as assessed by the genesis of arthritis and carditis or long-term persistence of pathogens in mice o

72 GlcNAc/anti-myosin mAb 3.B6 from a rheumatic carditis patient was cytotoxic for human endothelial cel

73 king a subset of MAbs derived from rheumatic carditis patients that bind both myosin and streptococca

74 Carditis regressed in immunocompetent mice and those lac

75 Our results show that carditis regresses in B-cell-deficient B10.A(k) mice but

76 cell-mediated immunity may be important for carditis regression.

77 ted alphabeta T-cell-deficient mice promoted carditis resolution.

78 of IL-10 during infection of arthritis- and carditis-susceptible C3H mice.

79 phages comprise the principal immune cell in carditis, T-cell responses that augment cell-mediated im

80 ts that cardiac myosin epitopes in rheumatic carditis target the S2 region of cardiac myosin and are

81 orreliosis is characterized by arthritis and carditis that are most severe at 2 to 3 wk, then regress

82 eliably produces an infectious arthritis and carditis that peak around 3 weeks postinfection and then

83 burgdorferi, results in acute arthritis and carditis that regress as a result of B. burgdorferi-spec

84 sent in autoimmune myocarditis and rheumatic carditis, the purpose of the current study was to determ

85 T cells modulate the severity of murine Lyme carditis through the action of IFN-gamma, which appears

86 ed infections and with ongoing arthritis and carditis, treatment selectively induced arthritis resolu

87 however, in the developing world, rheumatic carditis, Trypanosoma cruzi, and bacterial infections su

88 velopment of experimental Lyme arthritis and carditis via CXCR2-mediated recruitment of neutrophils i

89 The presence of cardiac epithelium and carditis was associated with deterioration of lower esop

90 In contrast, the resolution of carditis was delayed in CIITA-deficient animals compared

91 Murine Lyme carditis was not affected by either IL-11 or IL-11 antib

92 Development of disease (arthritis and carditis) was attenuated only in the early stage of infe

93 k between infections with GAS and autoimmune carditis, we studied the proliferative responses of PBMC

94 To investigate cardiac injury in borrelia carditis, we used antibody-deficient mice persistently i

95 c human T cell clones derived from rheumatic carditis were cross-reactive with human cardiac myosin,

96 i spirochetes that do not cause arthritis or carditis were developed and used to investigate Lyme dis

97 The anti-myosin mAbs from rheumatic carditis were found to react with specific peptides from

98 itis occurred more commonly in patients with carditis whose sphincter, on manometry, was structurally

99 role of IFNgamma in the development of Lyme carditis, wild-type and IFNgamma-deficient C57BL/6 mice

100 are similar among populations with rheumatic carditis worldwide, regardless of the infecting group A