Analysis Tools
immune system
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• in a IgE-dependent passive cutaneous anaphylaxis (PCA) model, homozygotes display enhanced susceptibility to IgE-mediated mast cell activation over a 10-fold range of IgE sensitizing concentrations in situ
• in a model of acute active cutaneous anaphylaxis, OVA-immunized homozygotes, but not wild-type mice, show robust ear swelling consisting of edema without a cellular infiltrate at 0.5 hrs after i.d. OVA challenge, suggesting an increased release of vasoactive mediators from mast cells
• in a model of active systemic anaphylaxis, homozygotes display a greater and accelerated susceptibility to anaphylactic death relative to wild-type mice, suggesting an augmented burst of mediator release from mast cells
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• in a IgE-dependent PCA model, homozygotes exhibit a 2-fold increase in mast cell degranulation at both 0.5 and 4 hrs after i.v. DNP-HSA challenge relative to wild-type mice, as noted histologically and quantified by intact mast cell counting
• in a model of acute active cutaneous anaphylaxis, OVA-immunized homozygotes exhibit a 4-fold increase in mast cell degranulation at 0.5 hrs after i.d. OVA challenge relative to wild-type mice, as noted histologically and quantified by intact mast cell counting
• in a model of active systemic anaphylaxis, where initial OVA immunization is followed by i.v. injection with 10 mg OVA, 2 of 3 homozygotes show (post-mortem) focal leukosequestration of neutrophils and mast cell degranulation in the trachea, as well as myocyte swelling and distorted myofibrils associated with mast cell degranulation in the heart
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• in a IgE-dependent PCA model, where i.d. ear injection of anti-DNP IgE is followed by treatment 20 hrs later with i.v. DNP-HSA, homozygotes show a 2- to 3-fold increase in net ear swelling at 0.5-2 hrs after challenge, as well as a 2-fold increase in mast cell degranulation at both 0.5 and 4 hrs after antigen challenge relative to wild-type mice
• in a model of active cutaneous anaphylaxis, where i.p. injection on days 0 and 5 with 10 g of chicken OVA is followed by treatment ~3 weeks later with i.d. ear injection of 50 ng OVA, homozygotes, but not wild-type mice, display robust ear swelling at 0.5 hrs that is somewhat greater than that noted by PCA with 25 ng of hapten-specific IgE, as well as tissue edema and a 4-fold increase in mast cell degranulation at 0.5 hrs after challenge relative to wild-type mice
• in a model of active systemic anaphylaxis, where initial OVA immunization is followed by i.v. injection with 10 mg OVA, homozygotes show a significantly higher and faster death rate, with 68% vs only 27% of wild-type dying after systemic antigen challenge, and mean survival times of 26 8 min and 45 9 min, respectively
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hematopoietic system
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• in a IgE-dependent passive cutaneous anaphylaxis (PCA) model, homozygotes display enhanced susceptibility to IgE-mediated mast cell activation over a 10-fold range of IgE sensitizing concentrations in situ
• in a model of acute active cutaneous anaphylaxis, OVA-immunized homozygotes, but not wild-type mice, show robust ear swelling consisting of edema without a cellular infiltrate at 0.5 hrs after i.d. OVA challenge, suggesting an increased release of vasoactive mediators from mast cells
• in a model of active systemic anaphylaxis, homozygotes display a greater and accelerated susceptibility to anaphylactic death relative to wild-type mice, suggesting an augmented burst of mediator release from mast cells
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• in a IgE-dependent PCA model, homozygotes exhibit a 2-fold increase in mast cell degranulation at both 0.5 and 4 hrs after i.v. DNP-HSA challenge relative to wild-type mice, as noted histologically and quantified by intact mast cell counting
• in a model of acute active cutaneous anaphylaxis, OVA-immunized homozygotes exhibit a 4-fold increase in mast cell degranulation at 0.5 hrs after i.d. OVA challenge relative to wild-type mice, as noted histologically and quantified by intact mast cell counting
• in a model of active systemic anaphylaxis, where initial OVA immunization is followed by i.v. injection with 10 mg OVA, 2 of 3 homozygotes show (post-mortem) focal leukosequestration of neutrophils and mast cell degranulation in the trachea, as well as myocyte swelling and distorted myofibrils associated with mast cell degranulation in the heart
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cellular
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• in a IgE-dependent PCA model, homozygotes exhibit a 2-fold increase in mast cell degranulation at both 0.5 and 4 hrs after i.v. DNP-HSA challenge relative to wild-type mice, as noted histologically and quantified by intact mast cell counting
• in a model of acute active cutaneous anaphylaxis, OVA-immunized homozygotes exhibit a 4-fold increase in mast cell degranulation at 0.5 hrs after i.d. OVA challenge relative to wild-type mice, as noted histologically and quantified by intact mast cell counting
• in a model of active systemic anaphylaxis, where initial OVA immunization is followed by i.v. injection with 10 mg OVA, 2 of 3 homozygotes show (post-mortem) focal leukosequestration of neutrophils and mast cell degranulation in the trachea, as well as myocyte swelling and distorted myofibrils associated with mast cell degranulation in the heart
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