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The Cause Of Hypersensitivity Reactions And Allergy

May 29, 2008
Millions of Canadians suffer from allergies and asthma. When your immune system identifies a normally harmless material as a threat, it can set off symptoms like sniffles, sneezes, rashes or breathing problems.

Although allergies and colds have similar symptoms, there are some telltale signs that can help you differentiate between them. If you aren't sure whether you have allergies or just a cold, ask your health professional. Your pharmacist or doctor can help determine the cause of your symptoms and recommend appropriate treatment.

Experts think that 1-2 percent of Canadians have serious allergies to food, insects, medications, latex, and exercise. These allergies are potentially life-threatening emergencies that require immediate medical attention.

A person experiencing a serious allergic reaction may have difficulty breathing, throat swelling, skin redness or itching, and an irregular heartbeat or palpitations. In most cases, it is recommended that people with an identified serious allergy wear a MedicAlert bracelet and carry an EpiPen, which is an injection device that contains epinephrine.

A recent study showed that two out of three parents were unsure of how to use their child's EpiPen, and almost half did not even carry their EpiPen with them at all times. If you or a family member have a serious allergy, talk to your pharmacist or doctor, and make sure you know how to recognize all the signs of a potentially life-threatening reaction so that you know exactly what to do if the time ever comes.

Delayed hypersensitivity reactions are inflammatory reactions initiated by mononuclear leukocytes. The term delayed is used to differentiate a secondary cellular response, which appears 48-72 hours after antigen exposure, from an immediate hypersensitivity response, which generally appears within 12 minutes of an antigen challenge. These reactions are mediated by T cells and monocytes/macrophages rather than by antibodies. They are also termed type IV hypersensitivity reactions.

Delayed hypersensitivity is a major mechanism of defense against various intracellular pathogens, including mycobacteria, fungi, and certain parasites, and it occurs in transplant rejection and tumor immunity. The central role of CD4+ T cells in delayed hypersensitivity manifests in patients with AIDS. Because of the loss of CD4+ cells, the host response against intracellular pathogens such as Mycobacterium tuberculosis is markedly impaired. The bacteria are engulfed by macrophages but are not killed.

If T-cell function is abnormal, the patient presents with opportunistic infections, including infection with mycobacteria, fungi, parasites, and, often, mucocutaneous candidiasis. Undesirable consequences of delayed-type hypersensitivity (DTH) reactions include illness such as contact dermatitis and allograft rejection.

Examples of DTH reactions are contact dermatitis (eg, poison ivy rash), tuberculin skin test reactions, granulomatous inflammation (eg, sarcoidosis, Crohn disease), allograft rejection, graft versus host disease, and autoimmune hypersensitivity reactions. Of note, the Rhus genus of plants, which includes poison ivy, poison oak, and poison sumac, all cause identical rashes.

The cellular events that result in delayed hypersensitivity reactions primarily involve T cells and macrophages. First, local immune and inflammatory responses at the site of foreign antigen up-regulate endothelial cell adhesion molecule expression, promoting the accumulation of leukocytes at the tissue site. The antigen is engulfed by macrophages and monocytes and is presented to a T cell that has a specific receptor for that antigen. Macrophages secrete interleukin (IL)1, IL-2, IL-6, and other lymphokines. Cytotoxic T cells can also be activated. The recruited macrophages can form giant cells. The characteristic histologic appearance of the macrophage T-cell infiltrate is a granuloma. This type of infiltrate in the tissue is called granulomatous inflammation.

Several variants of DTH exist, and their precise pathophysiologic mechanisms are slightly different. For example, in contact hypersensitivity reactions, the epidermis is involved; in pulmonary tuberculosis (TB), lung tissue is involved.

Delayed hypersensitivity reactions are normal physiological events. Anything that alters these normal events can lead to multiple opportunistic infections. Immune deficiencies (congenital or acquired) and immunosuppressive agents can alter this normal response.

he cellular events that result in delayed hypersensitivity reactions primarily involve T cells and macrophages. First, local immune and inflammatory responses at the site of foreign antigen up-regulate endothelial cell adhesion molecule expression, promoting the accumulation of leukocytes at the tissue site. The antigen is engulfed by macrophages and monocytes and is presented to a T cell that has a specific receptor for that antigen.

Macrophages secrete IL-1, IL-2, IL-6, and other lymphokines. Cytotoxic T cells can also be activated. The recruited macrophages can form giant cells. The characteristic histologic appearance of the macrophage T-cell infiltrate is a granuloma. This type of infiltrate in the tissue is called granulomatous inflammation.
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