For individuals with severe asthma, the potential for fatal bronchospasm throughout peanut-related anaphylaxis was 6.8 times greater in comparison to individuals with mild asthma. Those with mild asthma only had a 2.7-fold higher risk for fatal bronchospasm in comparison to children with no asthma. Airways pathways are believed to be bombarded with an increase in basophils, mast cells, eosinophils and neutrophils in response to becoming activated upon exposure to peanuts allergen …show more content…
The antigens are then offered to MHC class II receptors, which are identified by cell receptors on T-cell. In conjunction with IL-4, this will elicit their differentiation into CD4+ Th2 cells. These Th2 cells multiply and discharge pro-inflammatory cytokines, such as IL-4, IL-5, and IL-13, which may attach to B cells of the IgM subtype or undifferentiated B cells. This coupling results in their differentiation into IgE, which have a high affinity for FCER1 on mast cells, basophils, and eosinophils. Once peanut allergens infiltrate mucosal barriers peanut allergens and cell-bound IgE crosslink. This causes the degranulation of preformed allergic mediators and subsequent cell activation, which recruits potent cytokines and chemokines to become active; thus, mediating an inflammation response by histamine and the resultant symptoms typical of allergy. While numerous foods may elicit clinical syndromes in susceptible individuals, the allergic reaction elicited by peanuts is exclusively an IgE-mediated type I hypersensitivity