Rebekka, an 18-year-old college student, used to have a mildly runny and stuffy nose, mostly in the fall. On Labor Day weekend, she spent several hours at an outdoor barbecue and developed episodes of sneezing, a runny nose and itchy and watery eyes. She wondered “Am I allergic to something in the air? But why isn’t Bridget?”
What is an allergy? An allergy is defined as an “abnormal sensitivity to a substance normally tolerated and generally considered harmless substances such as pollen, food, drugs or even insect sting. This means that while some substances are as a rule well tolerated by most people, they can induce an adverse reaction (allergic reaction) in others, mainly due to the presence of the IgE antibody.
What is an IgE antibody? The first we need understand is our immune system. B lymphocytes, with the help of T lymphocytes and macrophages, can produce five separate and distinct classes of immunoglobulin (antibodies), IgA, IgG, IgM, IgD and IgE. IgA, IgG and IgM, the immunoglobulins that protect our bodies against foreign organisms, are produced by almost everyone except for some people with congenital or acquired immunodeficiency. IgD plays a non-significant role in the immune process.
Despite its presence in our body in only minute quantity, the antibody that is a key player in allergic reactions is the IgE. The reason why some substances (allergens) have the ability to induce IgE production, and others substances (non-allergens) do not, or why only some individuals develop an allergic reaction after exposure to some particular allergens is still not fully understood. However, we do know that genetic predisposition plays a significant role in developing allergic conditions. For example, children whose parents have allergic rhinitis or asthma have a significantly increased likelihood of developing allergic rhinitis and asthma.
Take Rebekka’s case. Her mother has a history of eczema and allergic asthma. Rebekka inherited the ability to produce IgE to ragweed, but did not experience a reaction the first time she was exposed to ragweed. However, after re-exposure for a period of time, she produced ragweed-IgE that bound themselves to the surface mast and basophil cells in the lining of her nose and conjunctiva. In other words, she was already sensitized to ragweed. After being re-exposed to ragweed, the mast and basophil cells immediately released a variety of potent chemical mediators (histamine, leukotriene and prostaglandins) and made her itch and sneeze, and made her nose stuffy and runny and eyes watery and itchy: an allergic reaction.
Unlike Rebekka, Bridget did not produce ragweed-IgE and had no problems. For her, ragweed is not an allergen and would not cause her symptoms, so outdoor activity during ragweed season can be a walk in the park.