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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

20 Immediate hypersensitivity is common in children with Eo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

38 In immediate hypersensitivity reactions, IgE effector funct

39 During IgE-mediated immediate hypersensitivity reactions, vascular endotheli

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

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

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

43 Immediate hypersensitivity reflects the permanent sensit

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

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

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

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

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

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

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

51 Immediate hypersensitivity to antivenoms often occurs du

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

53 Immediate hypersensitivity to cockroach, house-dust-mite

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

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

56 Immediate hypersensitivity to indoor or outdoor allergen

57 In conclusion, immediate hypersensitivity to moxifloxacin might involve

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

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

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