Disease relevance of Hypersensitivity, Immediate

• Infantile agammaglobulinemia and immediate hypersensitivity to penicillin G [1].
• BACKGROUND: Immediate hypersensitivity to latex, induced by natural latex proteins remaining on the finished products, may lead to severe anaphylactic reactions [2].
• Generalized urticaria to cyclophosphamide: Type I hypersensitivity to an immunosuppressive agent [3].
• Food allergy was documented by history, positive skin tests for immediate hypersensitivity, radioallergosorbent test, histamine release studies, and lymphocyte transformation in response to food allergens [4].
• Mediators released during the immediate hypersensitivity reaction may attract neutrophils and other chemotactic factors involved in the late allergic response, which includes a recrudescence of MCA caused by the release of histamine-releasing factors [5].

High impact information on Hypersensitivity, Immediate

• To address the hypothesis that stimulated leukotriene synthesis causes symptoms of immediate-hypersensitivity reactions in vivo, I investigated the effects of a new 5-lipoxygenase inhibitor, A-64077, on provoked allergic nasal symptoms and mediator release in a double-blind, randomized, placebo-controlled study [6].
• Transfer of allergen-specific IgE-mediated hypersensitivity with allogeneic bone marrow transplantation [7].
• Mediators of immediate hypersensitivity derived from arachidonic acid [8].
• Such contact leads to the activation of mast cells and the release of histamine and other pharmacological mediators, causing an immediate hypersensitivity and acute inflammatory reactions, accompanied by the development of allergic symptoms [9].
• Leukotrienes C4, D4, and E4, which are released from the lung tissue of asthmatic subjects exposed to specific allergens, seem to play a pathophysiological role in immediate hypersensitivity reactions [10].

Chemical compound and disease context of Hypersensitivity, Immediate

• Because of the close temporal association of events, operative mechanisms may be either an immediate hypersensitivity reaction to some components of wasp venom or a direct toxic effect of these substances on acetylcholine synthesis, release, or degradation [11].
• The relase of the BK-A is calcium and temperature dependent, requires metabolic energy, and is controlled by hormone-receptor interactions that influence the cellular level of cyclic AMP, as has been described for other mediators of immediate hypersensitivity reactions [12].
• Immediate hypersensitivity to aztreonam [13].
• This endogenous source of adenosine may act locally through a positive feedback mechanism to potentiate immediate hypersensitivity reactions [14].
• Atopic hypersensitivity to cis-dichlorodiammineplatinum(II) and other platinum complexes [15].

Biological context of Hypersensitivity, Immediate

• The results show that IgG2b antibody production in response to T1699 syngeneic tumor antigens is thymus independent and suggest that this antibody is the mediator of immediate hypersensitivity [16].
• This effect of IL 1 provides a mechanism for non-IgE-related local HA release and raises the possibility of a link between cellular immunity and immediate hypersensitivity of potential importance for the pathology of immuno/inflammatory diseases [17].
• Induction of type I hypersensitivity in guinea pigs after inhalation of phthalic anhydride [18].
• This represents the first complete amino acid sequence of a ragweed allergen and it should provide a basis for many structure-function correlative experiments in the field of immediate hypersensitivity [19].
• CONCLUSIONS: These results suggest that the identification of reactions of immediate hypersensitivity mediated by antilatex antibodies in HCW should be encouraged to prevent occupational exposure to latex products [20].

Anatomical context of Hypersensitivity, Immediate

• Anaphylactic relase of a basophil kallikrein-like activity. II. A mediator of immediate hypersensitivity reactions [12].
• Specific V beta T cell subsets mediate the immediate hypersensitivity response to ragweed allergen [21].
• These results suggest that histamine may participate in the recruitment of eosinophils during immediate hypersensitivity reactions [22].
• The pathogenetic role of allergy in chronic otitis media with effusion appears to be related to an exaggerated immediate hypersensitivity response to an allergen and/or infectious agent leading to dysfunction of the eustachian tube [23].
• Immediate hypersensitivity reactions in the intestinal mucosa evoke active chloride secretion which enhances the elimination of luminal antigens [24].

Gene context of Hypersensitivity, Immediate

• Macrophage inflammatory protein-1alpha as a costimulatory signal for mast cell-mediated immediate hypersensitivity reactions [25].
• Selective inhibition of IL-4 may be beneficial in T-helper cell type 2-dominated diseases, like type I hypersensitivity reactions or helminthic infections [26].
• Genetic and biochemical evidence for a critical role of Janus kinase (JAK)-3 in mast cell-mediated type I hypersensitivity reactions [27].
• Antagonistic site II mutants of human IL-4 are therefore effective inhibitors with therapeutic potential for IL-4 associated diseases like type I hypersensitivity and asthma [28].
• They further suggest a pathophysiological role for FKBP12 as a mediator in immediate or type I hypersensitivity and may have implications for novel therapeutic strategies in the treatment of allergic disorders with FK506 and rapamycin [29].

Analytical, diagnostic and therapeutic context of Hypersensitivity, Immediate

• It is suggested that terfenadine should be stopped at least three days before performing skin tests for type I hypersensitivity [30].
• Specific immunotherapy (SIT) is the practice of administering increasing doses of allergen extracts to selected subjects suffering from IgE-mediated hypersensitivity, with the ultimate aim of ameliorating the symptoms associated with exposure to the causative allergen [31].
• Thirty patients infected with Schistosoma mekongi, S. mansoni or S. japonicum had cell-mediated immune responses assessed by lymphocyte transformation in vitro (LT), immediate hypersensitivity responses determined by basophil histamine release in vitro (HR) and IgG antibody responses evaluated in an enzyme-linked immunosorbent assay (ELISA) [32].
• This patient, like most patients with immediate hypersensitivity reactions to methotrexate, developed recurrent symptoms during rechallenge of this agent despite prophylactic premedication [33].
• BACKGROUND: We report a documented grade III IgE-mediated hypersensitivity reaction associated with the use of 2.5% patent blue V dye for sentinel lymph node biopsy during breast cancer surgery [34].

References