Hypersensitivity can be defined as the exaggerated activity of the immune system against environmental antigens (allergy), or a misdirected activity against the host’s cells, referred to as autoimmunity. Isoimmunity is the activity of the immune system that is usually directed towards the body’s vital organs. Type one hypersensitivity is an immunoglobulin E-mediated allergic reaction. This paper looks at the mechanisms by which helper 2 T cells, mast cells and eosinophils coordinate to cause the signs and symptoms of type one hypersensitivity.

Type 1 hypersensitivity reaction is mediated by pre-formed mediators histamine, interleukin 1, TNF alpha and interleukin 6. There are also secondary mediators like prostaglandins and leukotrienes, and the Th2 cytokines like interleukin 4 and 5. The mast cells are responsible for controlling the immediate response. On the other hand, the neutrophils and eosinophils drive the late response (Stanley, 2002). and interleukin 4 which are necessary for the B-cell activation. Due to the production of their mediators by the basophils, mast cells, eosinophils and T2 helper cells, different organs of the body react differently, showing the effects of the hypersensitivity. The digestive tract reacts through cramping, diarrhea and vomiting (Porth, 2011). The skin appears reddened and inflamed, resulting in itching. The sensitivity of the airway results in wheezing and asthma, or sneezing and rhinitis. The smooth muscle contraction and systemic vasodilation causes severe bronchial constriction, shock and edema. In essence, a type 1 hypersensitivity reactions are caused by the release of chemical substances by the mast cells, T2 helper cells, eosinophils and basophils.

References

Porth, C. (2011). Essentials of pathophysiology: Concepts of altered health states. Hoboken, NJ: Lippincot Williams & Wilkins.

Stanley, J. (2002). Essentials of immunology and serology. Stamford, CT: Cengage Learning.