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1 , preventing allergic airway disease upon re-exposure to allergen.
2 d AHR and lung eosinophilia after subsequent exposure to allergen.
3 tration, mimicking asthma phenotypes without exposure to allergen.
4 e tissue recruitment of leucocytes following exposure to allergens.
5 CS, inducing allergic asthma after postnatal exposure to allergens.
6 xpected dendritic cell (DC) maturation after exposure to allergens.
7 s were fundamental for IL-33 secretion after exposure to allergens.
8 ction that occurs within minutes to hours of exposure to allergens.
9 ms by which MCM is reduced despite continued exposures to allergen.
10 is crucial for reducing MCM during prolonged exposures to allergen.
11 lowed by four intranasal sensitizations, and exposure to allergen aerosol 3 hours per day, 3 days per
12 s viral and other respiratory infections and exposure to allergens, air pollutants, and active or pas
13    These observations suggest that following exposure to allergen, airway T cells are functionally bu
14                                              Exposure to allergen alone, diesel exhaust alone, or all
15 ed airway constriction triggered by repeated exposure to allergen, also called hyperreactivity, is a
16 s of distinguishing the role of occupational exposure to allergens, also present in non-occupational
17 g evidence that early life events, including exposure to allergen and infections, are critical in pro
18 y diverse roles in airway inflammation after exposure to allergens and infections.
19 acerbations are associated with the level of exposure to allergens and LPS.
20                                      Chronic exposure to allergens and other airborne antigens can re
21 assed parental history of allergy, potential exposure to allergens and stress, known to be associated
22 tivated intrapulmonarily after infections or exposures to allergen and C5 inhibition has profound eff
23 is an inflammatory disorder caused by airway exposures to allergens and chemical irritants.
24 o personal characteristics and environmental exposures to allergens and endotoxin and to the developm
25 ealth data, targeted interventions to reduce exposures to allergens and irritants, and research on th
26 nes, and the chemokines that are released on exposure to allergens, and the IgE pathway.
27               Our findings show that a short exposure to allergens as well as ongoing type 2 immune r
28                                  Respiratory exposure to allergens can lead to airway tolerance.
29     T-cell tolerance, induced by respiratory exposure to allergen, can inhibit the development of air
30                                              Exposure to allergens caused HBE cells to rapidly releas
31 chronic airway inflammatory disease in which exposure to allergens causes intermittent attacks of bre
32                                              Exposure to allergens crosslinks immunoglobulin E (IgE)
33                                              Exposure to allergens depends on multiple ecological str
34 ion is induced in airway epithelial cells by exposure to allergen-derived proteases and that PAR-2 is
35 bling, the authors examined the relations of exposure to allergens (dust mite, cockroach, cat, and do
36 atment with dexamethasone during respiratory exposure to allergen eliminated the development of IL-10
37                                 Furthermore, exposure to allergens enhanced airway smooth muscle laye
38               We sought to determine whether exposure to allergen, exposure to diesel exhaust (DE), o
39 e of hyporesponsiveness such that subsequent exposure to allergen failed to re-exacerbate asthmatic l
40                 Furthermore, after prolonged exposure to allergen, hyperplastic epithelial cells pers
41 erresponsiveness (AHR) after repeated airway exposure to allergen in sensitized mice.
42 ver, other cutaneous consequences of chronic exposure to allergens in implanted devices are not well
43     Moreover, animal models demonstrate that exposure to allergens in strongly sensitized mothers inf
44 gic sensitization, but it is unknown whether exposure to allergens in the home is associated with out
45                                  Respiratory exposure to allergen induces T cell tolerance and protec
46                                  Respiratory exposure to allergen induces T cell tolerance and protec
47 epithelial cells (AEC), and during prolonged exposure to allergen, mucous cell hyperplasia remained e
48 tudies of mice with skin barrier disruption, exposure to allergens on the skin induces food allergy.
49 tifactorial: the disease can be triggered by exposure to allergens or drugs, but a genetic background
50 mmatory or epithelial repair functions after exposure to allergens, pathogens, or chemical irritants.
51 provide the first evidence that epicutaneous exposure to allergens potently primes for EE via a Th2-d
52                                              Exposure to allergens produced by a variety of otherwise
53                                              Exposure to allergens produced by the German cockroach (
54 ominant feature, in human asthma, an initial exposure to allergen results in T(H)2 cell-dependent sti
55                                              Exposure to allergens, such as house dust mite (HDM), th
56  inflammatory flares resulting from repeated exposure to allergen that are a debilitating feature of
57                                           Re-exposure to allergen then activates mast cells, which re
58                                        Early exposure to allergens through a defect skin barrier has
59 nt factors, including repeated or persistent exposure to allergens, which can lead to Th2-cell expans
60  allergic subjects, persistent or repetitive exposure to allergens, which typically are intrinsically