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Mechanisms of Oral Tolerance Breakdown in Food Allergy

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Children's Hospital Corporation Boston United States

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Aim 1 Th2 and mast-cell mediated suppression of allergen-specific iTR cell response. The hypothesis is that the prevailinignTh2 environment II4raF709 mice suppresses the generation of allergen-specific iTR cells. Blockade of Th2 and mast cell pathways may not only inhibit anaphylaxis but also promote tolerance. Aim 2 capacity of mast cell depletion to restore oral tolerance in established allergic sensitization. The hypothesis is the mast cell expansion perpetuates oral intolerance to allergen, and that their acute depletion enables tolerance induction in established food allergy. Aim 3 allergen-specific TR cell therapy in the treatment of established oral sensitization. The hypothesis is that allergen-specific iTR cells of WT but not II4raF709 mice would rescue established oral allergic sensitization and suppress the Th-2 skewing and mast cell expansion.

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Technical Report,30 Sep 2011,31 Aug 2014



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Approved For Public Release;

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