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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  A fumigatus-sensitized patients with CF and ABPA when compared with those in A fumigatus-sensitized
7 : nonsensitized, A fumigatus-sensitized, and ABPA.
8 ith allergic bronchopulmonary aspergillosis (ABPA) and cystic fibrosis-ABPA patients, whereas A. fumi
9  of allergic bronchopulmonary aspergillosis (ABPA) and fungal sensitisation, but how these relate to
10  as allergic bronchopulmonary aspergillosis (ABPA) and severe asthma with fungal sensitization (SAFS)
11 ate allergic bronchopulmonary aspergillosis (ABPA) in cystic fibrosis (CF).
12 and allergic bronchopulmonary aspergillosis (ABPA) in overtly immunocompetent and atopic individuals,
13     Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity lung disease caused by the m
14     Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity lung disease characterized b
15     Allergic bronchopulmonary aspergillosis (ABPA) is a syndrome seen in patients with asthma and cys
16     Allergic bronchopulmonary aspergillosis (ABPA) is caused by a dominant Th2 immune response to ant
17     Allergic bronchopulmonary aspergillosis (ABPA) is caused by A fumigatus and is characterized by e
18     Allergic bronchopulmonary aspergillosis (ABPA) is characterized by an allergic immunological resp
19  of allergic bronchopulmonary aspergillosis (ABPA) is not well understood.
20 ugh allergic bronchopulmonary aspergillosis (ABPA) leads to deterioration of pulmonary function, the
21     Allergic bronchopulmonary aspergillosis (ABPA) results from the interactions of the Aspergillus a
22 ave allergic bronchopulmonary aspergillosis (ABPA) were identified.
23 /or allergic bronchopulmonary aspergillosis (ABPA), which affects pulmonary function and clinical out
24 ith allergic bronchopulmonary aspergillosis (ABPA).
25 tal allergic bronchopulmonary aspergillosis (ABPA).
26 s with CF infected with A. fumigatus develop ABPA.
27                                 Experimental ABPA was associated with severe peribronchial eosinophil
28 ique role in the progression of experimental ABPA.
29 ary aspergillosis (ABPA) and cystic fibrosis-ABPA patients, whereas A. fumigatus-sensitized allergic
30 ective of whether they meet the criteria for ABPA.
31            The majority of TCC isolated from ABPA patients, and specific for the Asp f 1 allergen of
32 ulose membranes and evaluated IgE binding in ABPA patient and control sera.
33                 Increased PPBP expression in ABPA and CCPA may be useful as a future diagnostic tool
34 gest a role for increased PPBP expression in ABPA and CCPA.
35 tion with or without colonization (including ABPA); (iii) severe sinusitis with or without aspirin-ex
36       In contrast, CD4+ T cells from the non-ABPA cohort did not mount enhanced Th2 responses in vitr
37  A. fumigatus colonization in the absence of ABPA remains unclear.
38 who met strict criteria for the diagnosis of ABPA and had normal sweat electrolytes (< or = 40 mmol/l
39  specific and sensitive for the diagnosis of ABPA in CF.
40  may not have full criteria for diagnosis of ABPA or may involve other fungi.
41    The reference standard for a diagnosis of ABPA was the criteria of the Cystic Fibrosis Foundation
42 ity (95% CI: 96%, 100%) for the diagnosis of ABPA.
43                   The clinical expression of ABPA results from the complex interaction of chronic col
44                       The immunopathology of ABPA, ABPM, and SAFS is incompletely understood.
45 h contribute to the immunopathophysiology of ABPA.
46 ion and hyperresponsiveness in this model of ABPA, but had no effect on IL-10 nor IgE levels.
47  gene expression profile in a mouse model of ABPA.
48            Reports of familial occurrence of ABPA and increased incidence in CF patients suggest a po
49 ponses and their role in the pathogenesis of ABPA.
50 ypes are important in the pathophysiology of ABPA.
51  CFTR plays an etiologic role in a subset of ABPA patients.
52 llus fumigatus in conditions such as SAFS or ABPA may have beneficial effects in preventing key aspec
53 l of vitamin D supplementation in preventing ABPA is only feasible with concurrent elimination of A.
54 n levels were significantly increased in the ABPA (19.7-fold) and CCPA (27.7-fold) groups, compared w
55 otein levels were significantly lower in the ABPA and CCPA groups, compared with the healthy group, s
56             Heightened Th2 reactivity in the ABPA cohort correlated with lower mean serum vitamin D l
57 19.8%) were significantly increased in these ABPA patients.
58 y of T cell clones (TCC) isolated from three ABPA patients, and specific for a dominant Ag of A. fumi
59 tablished from the peripheral blood of three ABPA patients.
60 eutic trial of vitamin D to prevent or treat ABPA in patients with CF.
61  patients can occur in some individuals with ABPA.
62 lution of IMIS was observed in patients with ABPA after 3 months of specific treatment that was signi
63 ation]; range, 6-53 years): 18 patients with ABPA and 90 patients without ABPA.
64    Genetic risks identified in patients with ABPA include HLA association and certain T(H)2-prominent
65  the T-cell immune response in patients with ABPA is skewed to a T helper 2 cytokine secretion profil
66 ocyte-derived macrophages from patients with ABPA or CCPA and asthmatic and healthy controls (10 indi
67 y of the deltaF508 mutation in patients with ABPA was significantly higher than in 53 Caucasian patie
68 l blood mononuclear cells from patients with ABPA with the classically described A. fumigatus allerge
69  immunomodulating therapies in patients with ABPA, ABPM, and SAFS requires additional larger studies.
70 ly colonized by A fumigatus in patients with ABPA.
71  to be partially successful in patients with ABPA.
72 responses by CD4+ T cells from patients with ABPA.
73 ral CD4+ T cells isolated from patients with ABPA.
74 ntibody binding with sera from patients with ABPA.
75 gatus-colonized CF patients with and without ABPA to identify factors mediating tolerance versus sens
76 d and nonsensitized patients with CF without ABPA.
77 8 patients with ABPA and 90 patients without ABPA.

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