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 conate ameliorated inflammatory responses to inhaled allergen.

3 l lung disease caused by sensitization to an inhaled allergen.

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

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

6 ulates the balance of T(H) cell responses to inhaled allergen.

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

8 dditional role in modulating responses to an inhaled allergen.

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

10 atory airway responses following exposure to inhaled allergen.

11 arly and late bronchoconstrictor response to inhaled allergen.

12 ergic asthma is mediated by Th2 responses to inhaled allergens.

13 to be understood how CSF1R(+)cDC2s recognize inhaled allergens.

14 emory T cells and thus allergic responses to inhaled allergens.

15 b(+) cDC2s confer immunological tolerance to inhaled allergens.

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

17 tion and tissue remodeling after exposure to inhaled allergens.

18 sociated with increased sensitization toward inhaled allergens.

19 asthma by priming allergic sensitization to inhaled allergens.

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

21 he development of airway hypersensitivity to inhaled allergens.

22 caused by immunologic reactions to ingested/inhaled allergens.

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

24 nistering an allergen to induce tolerance to inhaled allergens.

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

26 ater development of elevated specific IgE to inhaled allergens, a positive skin prick test, and aller

27 Repeated exposure of mice to inhaled allergen activated the nuclei of solitary tract

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

29 These animals become sensitized to inhaled allergens and display normal responses in a shor

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

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

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

33 immunoglobulin E (IgE)-mediated reactions to inhaled allergens and is one of the most common chronic

34 The upper airways present a barrier to inhaled allergens and microbes, which alter immune respo

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

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

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

38 t a secondary or tertiary recall response to inhaled allergen, anti-CD3 inhibited all phenotypes of e

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

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

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

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

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

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

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

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

47 9 with airway hyperresponsiveness) underwent inhaled allergen challenge after 2-hour exposures to DE,

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

49 ivity and mucus metaplasia in response to an inhaled allergen challenge in sensitized mice.

50 acrophage function; however, its role during inhaled allergen challenge is not clear.

51 Inhaled allergen challenge was done before and after 4 w

52 cts had clinical reactivity quantified using inhaled allergen challenge), peanut allergic (n = 30, of

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

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

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

56 y was to define the role of itaconate during inhaled allergen challenge.

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

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

59 ving asthmatic airway inflammation following inhaled allergen challenge.

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

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

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

63 Inhaled allergen challenges and skin tests were conducte

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

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

66 ted whether targeting CD3 during exposure to inhaled allergen could prevent the accumulation of lung-

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

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

69 dministered at 30 minutes and 24 hours after inhaled allergen/diluent challenge.

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

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

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

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

74 ilic allergic lung inflammation triggered by inhaled allergens have not been fully elucidated.

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

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

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

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

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

80 ived TGF-B1 regulates pathogenic immunity to inhaled allergen in early life.

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

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

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

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

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

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

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

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

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

90 Exposure to inhaled allergens leads to increases in airway hyperresp

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

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

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

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

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

96 Inhaled allergens, pollutants, and respiratory viruses,

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

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

99 threshold for pathogenic immune responses to inhaled allergens remains unclear.

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

101 ls were employed, and mice were subjected to inhaled allergen sensitization with multiple readouts of

102 Inhaled allergen significantly increased mDC and pDC num

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

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

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

106 In response to provocation with inhaled allergens, the subsets of AMs are dynamically ch

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

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

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

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

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

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

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

114 sease caused by aberrant immune responses to inhaled allergens, which leads to airway hyperresponsive