ライフサイエンスコーパス: inhaled allergen

1 nduced by dendritic cells (DCs) that present inhaled allergen.

2 early- and late-phase allergic responses to inhaled allergen.

3 atopic asthma (n = 13) were challenged with inhaled allergen.

4 ment, and survival of T cells in response to inhaled allergen.

5 dditional role in modulating responses to an inhaled allergen.

6 h are recruited into the lung in response to inhaled allergen.

7 atory airway responses following exposure to inhaled allergen.

8 arly and late bronchoconstrictor response to inhaled allergen.

9 showed an increase in Th2 cell responses to inhaled allergens.

10 tion and tissue remodeling after exposure to inhaled allergens.

11 sociated with increased sensitization toward inhaled allergens.

12 asthma by priming allergic sensitization to inhaled allergens.

13 th increased serum IgE levels in response to inhaled allergens.

14 he development of airway hypersensitivity to inhaled allergens.

15 caused by immunologic reactions to ingested/inhaled allergens.

16 ic responses, and contribute to tolerance to inhaled allergens.

17 nistering an allergen to induce tolerance to inhaled allergens.

18 nt of deleterious type 2 immune responses to inhaled allergens.

19 sive and active barrier when encountering an inhaled allergen and how this double role contributes to

20 phagus and demonstrate an etiologic role for inhaled allergens and eosinophils in gastrointestinal in

21 e in allergic lung diseases by responding to inhaled allergens and initiating allergic inflammation.

22 Allergic asthma is caused by inhaled allergens and is characterized by airway eosinop

23 y life innate immune responses to ubiquitous inhaled allergens and PAMPs may influence asthma suscept

24 isrupt normal resistance to sensitization to inhaled allergens, and can thereby promote development o

25 al role in the orchestration of responses to inhaled allergens, and may contribute to the pathogenesi

26 y of Th2, Th17, and Treg immune responses to inhaled allergen are dependent on the quantity of LPS in

27 e infiltration of eosinophils in response to inhaled allergens are formidable obstacles to a larger u

28 Adaptive immune responses to inhaled allergens are induced following CCR7-dependent m

29 Sensitization to inhaled allergens at an early age (4 years) precedes the

30 red to act only as a physical barrier toward inhaled allergens, but also to actively contribute to ai

31 no detectable specific IgE responses to any inhaled allergens by MAST-26 may be still sensitized to

32 ory milieu might facilitate sensitization to inhaled allergens by the presence of mature dendritic ce

33 We compared responses to inhaled allergen challenge 24 h before the first injecti

34 asthmatics underwent methacholine challenge, inhaled allergen challenge and endobronchial allergen pr

35 Inhaled allergen challenge was done before and after 4 w

36 After inhaled allergen challenge, 9 days after treatment, the

37 methacholine challenge, on Day 3 they had an inhaled allergen challenge, and on Days 4 and 6 they had

38 The effects of treatment on responses to inhaled allergen challenge, sputum eosinophils, and airw

39 r the curve of FEV1 measured 2-8 h following inhaled allergen challenge.

40 ung inflammation than did wild-type DC after inhaled allergen challenge.

41 ving asthmatic airway inflammation following inhaled allergen challenge.

42 d to the lungs of naive recipients following inhaled allergen challenge.

43 effect on the late asthmatic reaction after inhaled allergen challenge.

44 in 11 patients with mild atopic asthma after inhaled allergen challenge.

45 Inhaled allergen challenges and skin tests were conducte

46 ild atopic asthma underwent methacholine and inhaled allergen challenges, and endobronchial allergen

47 h) and late (4-10 h) asthmatic responses to inhaled allergen compared with placebo.

48 Thus, isolated LAR induced by inhaled, allergen-derived peptides represent a novel mod

49 th asthma who have specific IgE responses to inhaled allergens detected by ImmunoCAP, which is not de

50 ral changes in the airways following chronic inhaled allergen exposure.

51 development of in vivo allergic responses to inhaled allergen exposure.

52 Timothy grass (TG) pollen is a well-studied inhaled allergen for which major IgE-reactive allergens

53 Exposure to inhaled allergens generates T helper 2 (Th2) CD4(+) T ce

54 the mechanisms by which IL-4 primes for new inhaled allergens: "IL-4-dependent pulmonary priming" re

55 enuates the early and late phase response to inhaled allergen in allergic asthmatic subjects.

56 ody does not inhibit the airway responses to inhaled allergen in allergic asthmatic subjects.

57 esses the early- and late-phase responses to inhaled allergen in allergic asthmatic subjects.

58 ion facilitates neosensitization to a second inhaled allergen in an IL-4-dependent manner and provide

59 siveness, and the late asthmatic reaction to inhaled allergen in patients with mild asthma.

60 oCAP detected specific IgE responses to some inhaled allergens in 27.1% of the patients.

61 ects of air pollution on immune responses to inhaled allergens in developing lungs by using very youn

62 tly to the understanding of sensitization to inhaled allergens in healthy airways but hardly any stud

63 o one or more inhaled allergens, the role of inhaled allergens in the induction of wheeze in the firs

64 by MAST-26 may be still sensitized to common inhaled allergens, including cockroach and moth.

65 iming the adaptive type 2 immune response to inhaled allergens, including the recruitment of eosinoph

66 DM allergen, particularly when the amount of inhaled allergen is low, by expanding allergen-specific

67 ics with a documented late-phase response to inhaled allergen (LAR).

68 Exposure to inhaled allergens leads to increases in airway hyperresp

69 en specific IgE antibodies towards 14 common inhaled allergens (MAST-26) were measured.

70 on during early- and late-phase responses to inhaled allergen might be driven at least in part by TSL

71 The effects of inhaled allergens on the expression of IL-17RB by mDCs a

72 e first cell layer to come into contact with inhaled allergens, our study implies CD23-mediated IgE t

73 rier dysfunction that implicates the size of inhaled allergen particles as an important factor influe

74 s) = 0.61) in BAL fluid and late response to inhaled allergen (r(s) = 0.51).

75 of allergic airway inflammation triggered by inhaled allergens remains unclear.

76 that activation of TLR3 in combination with inhaled allergen results in induction of dendritic cell

77 Inhaled allergen significantly increased mDC and pDC num

78 further assessment of their sensitization to inhaled allergens such as cockroach and moth using Immun

79 ucial players in TH2 sensitization to common inhaled allergens that enter the body through the skin a

80 dhood asthmatics are allergic to one or more inhaled allergens, the role of inhaled allergens in the

81 er integrity and enable a passive passage of inhaled allergens through the airway epithelium.

82 Our data support that impaired clearance of inhaled allergens triggering IL-13 production by multipl

83 or whom information on IgEs against 8 common inhaled allergens was available, collected at age 4 and

84 h IL-4 mediates allergic airway responses to inhaled allergens, we compared the effects of antigen se

85 airways in allergic diseases are exposed to inhaled allergens, we evaluated whether eosinophils with

86 EV on the development of hypersensitivity to inhaled allergens were also evaluated after airway sensi

87 and specific IgE antibodies towards 14 major inhaled allergens were measured.