This patient is experiencing the early phase of type I hypersensitivity, characterized by pruritus and watery discharge from the nose, bronchospasm, mucus secretion in the airways, and a wheal-and-flare response with pruritus in the skin. The mechanism of hypersensitivity involves prior sensitization of a population of TH2 cells that produced cytokines, including interleukin-4. The interleukin-4 causes B cells to switch their heavy chain class from IgM to IgE. The IgE molecules then attach to mast cells or basophils. With subsequent antigen (allergen) challenge, the mast cells degranulate and release mediators, including histamine, which produces the anaphylactic response. Eosinophils are involved in type I hypersensitivity reactions as well as type II antibody-dependent cell cytotoxicity reactions directed against parasites. Eosinophils enter the area of the reaction due to the release of eosinophil chemotactic factor (eotaxin) and the beta-chemokine RANTES released from TH2 CD4+ cells and mast cells. Eosinophils are recruited into the tissues as pa of the late-phase reaction of type I hypersensitivity. Their survival in tissue is dependent upon IL-3, IL-5, and granulocyte-monocyte colony stimulating factor (GM-CSF) released from TH2 cells. Megakaryocytes are bone marrow cells that produces platelets. They are not involved in type I hypersensitivity. Neutrophils are not a cell type that is key to the development of type I hypersensitivity. Ref: Brooks G.F., Carroll K.C., Butel J.S., Morse S.A., Mietzner T.A. (2013). Chapter 8. Immunology. In G.F. Brooks, K.C. Carroll, J.S. Butel, S.A. Morse, T.A. Mietzner (Eds), Jawetz, Melnick, & Adelberg's Medical Microbiology, 26e.