ライフサイエンスコーパス: immediate hypersensitivity

1 red for MC degranulation and serves to limit immediate hypersensitivity.

2 cells play a critical role in IgE-dependent immediate hypersensitivity.

3 d and serve as mediators of inflammation and immediate hypersensitivity.

4 mediators, a critical event in the onset of immediate hypersensitivity.

5 on, resulting in the release of mediators of immediate hypersensitivity.

6 , 1.7; 95% CI: 1.06-1.92; p = .001), but not immediate hypersensitivity.

7 diate the allergic reaction characterized by immediate hypersensitivity, a manifestation of IgE memor

8 flammatory mediators by mast cells in type 1 immediate-hypersensitivity allergic reactions relies on

9 that inflammatory mediators released during immediate hypersensitivity (allergic) reactions can prod

10 Mast cells are typically linked to immediate hypersensitivity and anaphylaxis.

11 Mast cells are the main effector cells of immediate hypersensitivity and anaphylaxis.

12 Reactions resulting from immediate hypersensitivity and cell-mediated processes w

13 Mast cells are the major effector cells for immediate hypersensitivity and chronic allergic reaction

14 variety of inflammatory conditions including immediate hypersensitivity and interstitial cystitis, th

15 mast cell activation plays a central role in immediate hypersensitivity and other allergic reactions.

16 t cells are the major effector-cell type for immediate hypersensitivity and other forms of allergic r

17 s (the discovery cohort) with a diagnosis of immediate hypersensitivity and the main finding was repl

18 ed mechanisms of action of IgE in pathologic immediate hypersensitivity, as well as its multifaceted

19 ng that HLA-DRB1*10:01 increased the risk of immediate hypersensitivity at a genome-wide level (odds

20 ith short ragweed pollen developed cutaneous immediate hypersensitivity but rejected corneal allograf

21 s with delayed hypersensitivity and 315 with immediate hypersensitivity compared to 1,308 controls.

22 gs, sensitivity of skin testing is higher in immediate hypersensitivity compared to nonimmediate hype

23 generated from patients with AX-Clav-induced immediate hypersensitivity diagnosed by positive skin te

24 ied based on the diagnosis of IgE-associated immediate hypersensitivity (EoE + IH vs. EoE-IH).

25 on with anti-IgE mAb suppressed IgE-mediated immediate hypersensitivity; however, some mice developed

26 Immediate hypersensitivity is common in children with Eo

27 as a proinflammatory role in asthma and skin immediate hypersensitivity, leading us to suggest HRF as

28 PD patients with dyskinesias display an immediate hypersensitivity of preSMA and putamen to levo

29 her not allergic in nature, are low risk for immediate hypersensitivity, or are a potential true alle

30 To understand the mechanism of the immediate hypersensitivity phenomenon, we need explanati

31 le participants were aged 7-16 years with an immediate hypersensitivity reaction after peanut ingesti

32 s with a suggestive history of a PPI-induced immediate hypersensitivity reaction and 30 control subje

33 dose at which objective signs/symptoms of an immediate hypersensitivity reaction developed) determine

34 a severe and potentially fatal IgE-dependent immediate hypersensitivity reaction to apparently harmle

35 In contrast to immediate hypersensitivity reactions (eg, anaphylaxis, u

36 sensus exists on the diagnostic approach for immediate hypersensitivity reactions (IHR) to radiocontr

37 Although IgE is a frequent cause of immediate hypersensitivity reactions (IHR), the role of

38 is known about the diagnostic approaches for immediate hypersensitivity reactions (IHRs) due to 5-nit

39 have been observed to predominantly trigger immediate hypersensitivity reactions (IHRs).

40 Iodinated contrast media produce non-immediate hypersensitivity reactions (NIHR).

41 ral rubber latex is a prerequisite to type I immediate hypersensitivity reactions (urticaria, angioed

42 lls are not only important effector cells in immediate hypersensitivity reactions and immune response

43 skin testing in the diagnosis of PPI-related immediate hypersensitivity reactions and the cross-react

44 Perioperative immediate hypersensitivity reactions are rare.

45 There were no reports of immediate hypersensitivity reactions caused by p55-IgG.

46 ing enzyme in many tissues, renin release in immediate hypersensitivity reactions could result in loc

47 a are generated during various IgE-dependent immediate hypersensitivity reactions in vivo.

48 are an increasing problem that involve both immediate hypersensitivity reactions mediated by IgE and

49 o mast cells through FcepsilonRI and trigger immediate hypersensitivity reactions on antigen encounte

50 E (IgE) antibodies are known for triggering immediate hypersensitivity reactions such as food anaphy

51 stration of some liposomal drugs can trigger immediate hypersensitivity reactions that include sympto

52 believed to be one of the major mediators of immediate hypersensitivity reactions that underlie atopi

53 duction of IgE, the Ab isotype that triggers immediate hypersensitivity reactions through the release

54 enetic associations have been discovered for immediate hypersensitivity reactions to beta-lactams, as

55 Patients with a clinical history of immediate hypersensitivity reactions to either penicilli

56 HLA-DRB1*10:01 predisposed to immediate hypersensitivity reactions to penicillins.

57 Immediate hypersensitivity reactions were reported in 9

58 In immediate hypersensitivity reactions, IgE effector funct

59 of gadoxetic acid adverse events, including immediate hypersensitivity reactions, NSF, and intracran

60 During IgE-mediated immediate hypersensitivity reactions, vascular endotheli

61 y lead to a higher frequency and severity of immediate hypersensitivity reactions.

62 hylaxis and other examples of IgE-associated immediate hypersensitivity reactions.

63 DRs to APs, 17% were classified as selective immediate hypersensitivity reactors by both clinical his

64 ed IgE production despite a relative lack of immediate hypersensitivity, recurrent infection, and an

65 Immediate hypersensitivity reflects the permanent sensit

66 X40 axis downregulates FcepsilonRI-dependent immediate hypersensitivity responses both in vitro and i

67 dicate that gp49B1 innately dampens adaptive immediate hypersensitivity responses by suppressing mast

68 as been implicated in negative regulation of immediate hypersensitivity responses.

69 Forty-two percent of subjects with immediate hypersensitivity skin test reactions to a Tric

70 higher in EoE + IH, regardless of eliciting immediate hypersensitivity symptoms.

71 n cohorts met the 20 + 2 rule despite absent immediate hypersensitivity symptoms; mature tryptase was

72 n cohorts met the 20 + 2 rule despite absent immediate hypersensitivity symptoms; mature tryptase was

73 st cells play as the major effector cells in immediate hypersensitivity through activation via the hi

74 Ag-specific IgE Abs not only mediate immediate hypersensitivity through mast cell activation,

75 Immediate hypersensitivity to antivenoms often occurs du

76 Patients with proven immediate hypersensitivity to AX (Group A) or CLV (Group

77 sive T-cells are detectable in patients with immediate hypersensitivity to AX-Clav, to assess whether

78 Immediate hypersensitivity to cockroach, house-dust-mite

79 he interplay between EoE- and IgE-associated immediate hypersensitivity to foods remains unclear.

80 Although asthma is strongly associated with immediate hypersensitivity to indoor allergens, several

81 Immediate hypersensitivity to indoor or outdoor allergen

82 In conclusion, immediate hypersensitivity to moxifloxacin might involve

83 nging trial in 84 patients with a history of immediate hypersensitivity to peanut.

84 ty compared with 20 patients with documented immediate hypersensitivity to penicillins recruited in I

85 autoimmunity to self, it may also encompass immediate hypersensitivity to self, which leads to shock

86 y to OX40L in wild-type mice caused enhanced immediate hypersensitivity, whereas the administration o