Type I (Anaphylactic) Reactions

Types of Hypersensitivity

Table 1

Type IV (Delayed Cell-Mediated) Reactions

Type III (Immune Complex) Reactions

Type II (Cytotoxic) Reactions

Type I (Anaphylactic) Reactions

Examples of Autoimmune Disease

The Origins of Autoimmune Disease

Genetic and Gender Correlation in Autoimmune Disease

Introduction

The term hypersensitivity refers to an antigenic response beyond that which is considered normal; the term allergy is more familiar and is essentially synonymous. Hypersensitivity responses occur in individuals who have been sensitized by previous exposure to an antigen, which in this context is sometimes called an allergen. When an individual who was previously sensitized is exposed to that antigen again, his or her immune system reacts to it in a damaging manner. There are four principal types of hypersensitivity reactions: anaphylactic, cytotoxic, immune complex, and cell-mediated (or delayed-type) reactions (Table1).

Type I, or anaphylactic, react ions often occur within 2 to 30 minutes after a person sensitized to an antigen is reexposed to that antigen. Anaphylaxis means opposite of protected," from the prefix ana-, meaning against, and the Greek phylaxis, meaning protection. Anaphylaxis is an inclusive term for the reactions caused when certain antigens combine with IgE antibodies. Anaphylactic responses can be systemic reactions, which produce shock and breathing difficulties and are sometimes fatal, or localized reactions, which include common allergic conditions such as hay fever, asthma, and hives (slightly raised, often itchy and reddened areas of the skin).

The IgE antibodies produced in response to an antigen, such as insect venom or plant pollen, bind to the surfaces of cells such as mast cells and basophils. These two cell types are similar in morphology and in their contribution to allergic reactions. Mast cells are especially prevalent in the connective tissue of the skin and respiratory tract and in surrounding blood vessels. The name is from the German word mastzellen, meaning “well fed”; they are packed with granules (Figure 1a). Basophils circulate in the bloodstream, where they constitute fewer than 1 % of the leukocytes. Both are filled with granules containing a variety of chemicals called mediators.

Figure 1a The mechanism of anaphylaxis. IgE antibodies, produced in response to an antigen, coat mast cells and basophils. When an antigen bridges the gap between two adjacent antibody molecules of the same specificity, the cell undergoes degranulation and releases histamine and other mediators.

Mast cells and basophils can have as many as 500,000 sites for IgE attachment. The Fc (stem) region of an IgE antibody can attach to one of these specific receptor sites on such a cell, leaving two antigen-binding sites free. Of course, the attached IgE monomers will not all be specific for the same antigen. But when an antigen such as plant pollen encounters two adjacent antibodies of the same appropriate specificity, it can bind to one antigen-binding site on each antibody, bridging the space between them. This bridge triggers the mast cell or basophil to undergo degranulation, which releases the granules inside these cells and also the mediators they contain (Figure 1 b).

Figure 1b The mechanism of anaphylaxis. A degranulated mast cell that has reacted with an antigen and released granules of histamine and other reactive mediators.

These mediators cause the unpleasant and damaging effects of an allergic reaction. The best-known mediator is histamine. The release of histamine increases the permeability and distension of blood capillaries, resulting in edema (swelling) and erythema (redness). Other effects include increased mucus secretion (a runny nose, for example) and smooth muscle contraction, which in the respiratory bronchi results in breathing difficulty.

Other mediators include leukotrienes of various types and prostaglandins. These mediators are not preformed and stored in the granules but are synthesized by the antigen-triggered cell. Because leukotrienes tend to cause prolonged contractions of certain smooth muscles, their action contributes to the spasms of the bronchial tubes that occur during asthmatic attacks. Prostaglandins affect smooth muscles of the respiratory system and increase mucus secretion.

Collectively, all these mediators serve as chemotactic agents that, in a few hours, attract neutrophils and eosinophils to the site of the degranulated cell. They then activate various factors that cause inflammatory symptoms, such as distension of the capillaries, swelling, increased secretion of mucus, and involuntary contractions of smooth muscles.

Дата добавления: 2015-06-04