Hypersensitivity

Type I (immunoglobulin E [IgE]-mediated reactions): (Allergic reaction)

 T helper 2 cells produce high levels of interleukin-4, leading to B-cell activation and subsequent plasma cell production of IgE antibody. IgE binds to mast cell receptors resulting in their immediate degranulation and release of histamine, leukotrienes, and other inflammatory mediators. (Your immune system overreacts to something harmless, makes IgE antibodies, and when exposed again, your mast cells release chemicals that cause allergic symptoms)

Examples: Allergic rhinitis, Asthma, Anaphylaxis

Type II (tissue-specific reactions): (Immune system is attacking its own cells)

Altered self-antigens on tissues are bound by autoantibodies resulting in tissue destruction by complement, macrophages, neutrophils, or natural killer cells. Some autoantibodies bind to hormone or neurotransmitter receptors causing decreased or increased receptor activation.(Your immune system mistakenly attacks your own body’s cells or changes how certain receptors work — which can damage tissues or cause abnormal cell function.)

Examples: Autoimmune hemolytic anemia, Heparin-induced thrombocytopenia, Graves disease, Myasthenia gravis

Type III (immune complex–mediated reactions):(Immune system forms clumps=damaging tissue)

 Antibodies are formed to circulating antigens resulting in the formation of immune complexes that deposit in tissues. These immune complexes activate complement and neutrophils resulting in tissue destruction. (Your body forms little clumps of immune material that get stuck in tissues, and the immune system’s attempt to clean them up ends up causing inflammation and damage.)

Examples: Systemic lupus erythematosus, Raynaud phenomenon

Type IV (cell-mediated reactions): (delayed hypersensitivity)

T helper 1 cells produce interferon gamma resulting in the activation of macrophages and T cytotoxic cells that attack the target cell through the release of destructive enzymes. In some cases, destruction of an invader is not possible, and granuloma formation walls it off from the rest of the body (Certain immune cells attack infected or abnormal cells directly. If they can’t kill the invader, they build a “wall” around it (a granuloma) to trap it and protect the rest of the body.)

Examples:Contact sensitivity to poison ivy and latex, Mycobacterial infection, TB

Manifestations of allergic reactions as a result of type I hypersensitivity include pruritus, angioedema (swelling caused by exudation), edema of the larynx, urticaria (hives), bronchospasm (constriction of airways in the lungs), hypotension (low blood pressure), and dysrhythmias (irregular heartbeat) because of anaphylactic shock, and gastrointestinal cramping caused by inflammation of the gastrointestinal mucosa. One of the most common type I reactions is asthma. It is presented in detail in Chapter 35. The central problem in asthma is obstruction of the large and small airways (bronchi) of the lower respiratory tract by bronchospasm (constriction of smooth muscle in airway walls), edema, and thick secretions. This leads to ventilatory insufficiency, wheezing, and difficult or labored breathing.

Urticaria, or hives, is a dermal (skin) manifestation of type I allergic reactions (see Fig. 9.6). The underlying mechanism is the localized release of histamine and increased vascular permeability, resulting in limited areas of edema. Urticaria is characterized by white fluid-filled blisters (wheals) surrounded by areas of redness (flares). The wheal and flare reaction is usually accompanied by itching. Not all urticarial symptoms are caused by allergic (immunologic) reactions. Some, termed nonimmunologic urticaria, result from exposure to cold temperatures, emotional stress, medications, systemic diseases, hyperthyroidism, or malignancies (e.g., lymphomas).