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The enormous survival value of the immune response is self‐evident. Adaptive immunity directed against a foreign material has as its ultimate goal the elimination of the invading substance. In the process, some tissue damage may occur as a result of the accumulation of components with nonspecific effects. This damage is generally temporary. As soon as the invader is eliminated, the situation at that site reverts to normal.

There are instances in which the power of the immune response, although directed against foreign substances—some innocuous such as some medications, inhaled pollen particles, or substances deposited by insect bites—produces a response that may result in severe pathological consequences and even death. These responses are known collectively as hypersensitivity reactions or allergic reactions. An understanding of the basic mechanisms underlying these disease processes has been fundamental in their treatment and control and, in addition, has contributed much to our knowledge of the normal immune response. The latter is true because both utilize essentially identical mechanisms; however, in hypersensitivity, these mechanisms are misdirected or out of control (see Chapters ).

Given the complexity of the immune response and its potential for inducing damage, it is self‐evident that it must operate under carefully regulated conditions, as does any other physiological system. These controls are multiple and include feedback inhibition by soluble products as well as cell–cell interactions of many types, which may either heighten or reduce the response. The net result is to maintain a state of homeostasis so that when the system is perturbed by a foreign invader, enough response is generated to control the invader, and then the system returns to equilibrium; in other words, the immune response is shut down. However, its memory of that particular invader is retained so that a more rapid and heightened response will occur should the invader return.

Disturbances in these regulatory mechanisms may be caused by conditions such as congenital defects, hormonal imbalance, or infection, any of which can have disastrous consequences. AIDS may serve as a timely example: it is associated with an infection of T lymphocytes that participate in regulating the immune response. As a result of infection with the human immunodeficiency virus (HIV), which causes AIDS, there is a decrease in occurrence and function of one vital subpopulation of T cells, which leads to immunological deficiency and renders the patient powerless to resist infections by microorganisms that are normally benign. An important form of regulation concerns the prevention of immune responses against self‐antigens. As discussed in Chapter 12, this regulation may be defective, thus causing an immune response against self to be mounted. This type of immune response is termed autoimmunity and is the cause of diseases such as some forms of arthritis, thyroiditis, and diabetes, which are very difficult to treat.