ライフサイエンスコーパス: ABPA

1 ABPA is the most common form of allergic bronchopulmonar

2 ABPA status was followed up for 1 year.

3 panbronchiolitis (1), congenital defect (1), ABPA (11), rheumatoid arthritis (4), and early childhood

4 Serotyping revealed that 16 of 18 ABPA patients were either HLA-DR2, HLA-DR5, or both.

5 Each ABP is a heterodimer assembled as an ABPA subunit encoded by an Abpa gene and linked by disul

6 ns, biomarkers, and management of asthma and ABPA, including a focus on SAFS, with the aim of updatin

7 A fumigatus-sensitized patients with CF and ABPA when compared with those in A fumigatus-sensitized

8 : nonsensitized, A fumigatus-sensitized, and ABPA.

9 Although pulmonary tuberculosis and ABPA are different illnesses, they share similarities in

10 ith allergic bronchopulmonary aspergillosis (ABPA) and cystic fibrosis-ABPA patients, whereas A. fumi

11 of allergic bronchopulmonary aspergillosis (ABPA) and fungal sensitisation, but how these relate to

12 of allergic bronchopulmonary aspergillosis (ABPA) and granulomatosis with polyangiitis (GPA).

13 as allergic bronchopulmonary aspergillosis (ABPA) and severe asthma with fungal sensitization (SAFS)

14 ith allergic bronchopulmonary aspergillosis (ABPA) are characterized by high frequencies of Th2 cells

15 and allergic bronchopulmonary aspergillosis (ABPA) do not rarely coexist and share several similariti

16 ate allergic bronchopulmonary aspergillosis (ABPA) in cystic fibrosis (CF).

17 and allergic bronchopulmonary aspergillosis (ABPA) in overtly immunocompetent and atopic individuals,

18 Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity lung disease caused by the m

19 Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity lung disease characterized b

20 Allergic bronchopulmonary aspergillosis (ABPA) is a lung disorder caused by immune-mediated react

21 Allergic bronchopulmonary aspergillosis (ABPA) is a syndrome seen in patients with asthma and cys

22 Allergic bronchopulmonary aspergillosis (ABPA) is caused by a dominant Th2 immune response to ant

23 Allergic bronchopulmonary aspergillosis (ABPA) is caused by A fumigatus and is characterized by e

24 Allergic bronchopulmonary aspergillosis (ABPA) is characterized by an allergic immunological resp

25 of allergic bronchopulmonary aspergillosis (ABPA) is not well understood.

26 ugh allergic bronchopulmonary aspergillosis (ABPA) leads to deterioration of pulmonary function, the

27 for allergic bronchopulmonary aspergillosis (ABPA) of Rosenberg and Patterson were not strictly satis

28 Allergic bronchopulmonary aspergillosis (ABPA) results from the interactions of the Aspergillus a

29 ave allergic bronchopulmonary aspergillosis (ABPA) were identified.

30 /or allergic bronchopulmonary aspergillosis (ABPA), which affects pulmonary function and clinical out

31 ith allergic bronchopulmonary aspergillosis (ABPA).

32 tal allergic bronchopulmonary aspergillosis (ABPA).

33 s with CF infected with A. fumigatus develop ABPA.

34 Experimental ABPA was associated with severe peribronchial eosinophil

35 ique role in the progression of experimental ABPA.

36 ary aspergillosis (ABPA) and cystic fibrosis-ABPA patients, whereas A. fumigatus-sensitized allergic

37 ective of whether they meet the criteria for ABPA.

38 ive Th2 cells as a potential risk factor for ABPA.FUNDINGGerman Research Foundation (DFG), under Germ

39 The majority of TCC isolated from ABPA patients, and specific for the Asp f 1 allergen of

40 negative, and thus the patient must have had ABPA from the onset.

41 ulose membranes and evaluated IgE binding in ABPA patient and control sera.

42 Increased PPBP expression in ABPA and CCPA may be useful as a future diagnostic tool

43 gest a role for increased PPBP expression in ABPA and CCPA.

44 tion with or without colonization (including ABPA); (iii) severe sinusitis with or without aspirin-ex

45 nd the challenges in diagnosing and managing ABPA.

46 In contrast, CD4+ T cells from the non-ABPA cohort did not mount enhanced Th2 responses in vitr

47 A. fumigatus colonization in the absence of ABPA remains unclear.

48 The first case of ABPA with comorbid GPA that developed exophthalmos is re

49 who met strict criteria for the diagnosis of ABPA and had normal sweat electrolytes (< or = 40 mmol/l

50 specific and sensitive for the diagnosis of ABPA in CF.

51 may not have full criteria for diagnosis of ABPA or may involve other fungi.

52 The reference standard for a diagnosis of ABPA was the criteria of the Cystic Fibrosis Foundation

53 ity (95% CI: 96%, 100%) for the diagnosis of ABPA.

54 The clinical expression of ABPA results from the complex interaction of chronic col

55 characteristics, and distinctive features of ABPA in the Indian subcontinent.

56 The immunopathology of ABPA, ABPM, and SAFS is incompletely understood.

57 h contribute to the immunopathophysiology of ABPA.

58 ociated with the diagnosis and management of ABPA in India.

59 ion and hyperresponsiveness in this model of ABPA, but had no effect on IL-10 nor IgE levels.

60 gene expression profile in a mouse model of ABPA.

61 Reports of familial occurrence of ABPA and increased incidence in CF patients suggest a po

62 ponses and their role in the pathogenesis of ABPA.

63 ypes are important in the pathophysiology of ABPA.

64 CFTR plays an etiologic role in a subset of ABPA patients.

65 hogenesis and the diagnosis and treatment of ABPA.

66 In the last two decades, most research on ABPA has been published from India.

67 llus fumigatus in conditions such as SAFS or ABPA may have beneficial effects in preventing key aspec

68 l of vitamin D supplementation in preventing ABPA is only feasible with concurrent elimination of A.

69 g and Patterson were not strictly satisfied, ABPA was diagnosed in conjunction with the course of tre

70 n levels were significantly increased in the ABPA (19.7-fold) and CCPA (27.7-fold) groups, compared w

71 otein levels were significantly lower in the ABPA and CCPA groups, compared with the healthy group, s

72 Heightened Th2 reactivity in the ABPA cohort correlated with lower mean serum vitamin D l

73 19.8%) were significantly increased in these ABPA patients.

74 y of T cell clones (TCC) isolated from three ABPA patients, and specific for a dominant Ag of A. fumi

75 tablished from the peripheral blood of three ABPA patients.

76 Though the pathogenesis common to ABPA and GPA remains unknown, neutrophilic inflammation

77 igher risk of irreversible damage related to ABPA and SAFS when compared to asthma alone.

78 eutic trial of vitamin D to prevent or treat ABPA in patients with CF.

79 The patient had been diagnosed with ABPA six years earlier, which had been repeatedly treate

80 patients can occur in some individuals with ABPA.

81 lution of IMIS was observed in patients with ABPA after 3 months of specific treatment that was signi

82 ation]; range, 6-53 years): 18 patients with ABPA and 90 patients without ABPA.

83 Genetic risks identified in patients with ABPA include HLA association and certain T(H)2-prominent

84 the T-cell immune response in patients with ABPA is skewed to a T helper 2 cytokine secretion profil

85 ocyte-derived macrophages from patients with ABPA or CCPA and asthmatic and healthy controls (10 indi

86 y of the deltaF508 mutation in patients with ABPA was significantly higher than in 53 Caucasian patie

87 l blood mononuclear cells from patients with ABPA with the classically described A. fumigatus allerge

88 immunomodulating therapies in patients with ABPA, ABPM, and SAFS requires additional larger studies.

89 ly colonized by A fumigatus in patients with ABPA.

90 to be partially successful in patients with ABPA.

91 responses by CD4+ T cells from patients with ABPA.

92 ral CD4+ T cells isolated from patients with ABPA.

93 ntibody binding with sera from patients with ABPA.

94 gatus-colonized CF patients with and without ABPA to identify factors mediating tolerance versus sens

95 d and nonsensitized patients with CF without ABPA.

96 8 patients with ABPA and 90 patients without ABPA.