Figure 4 Immune complex-mediated hypersensitivity

Delayed Cell-Mediated Hypersensitivity Reactions of the Skin

One delayed hypersensitivity reaction that involves the skin is the familiar skin test for tuberculosis. Because Mycobacterium tuberculosis is often located within macrophages, this organism can stimulate a delayed cell-mediated immune response. As a screening test, protein components of the bacteria are injected into the skin. If the recipient has (or has had) a previous infection by tuberculosis bacteria, an inflammatory reaction to the injection of these antigens will appear on the skin in 1 to 2 days.

Allergic contact dermatitis, another common manifestation of delayed cell-mediated hypersensitivity, is usually caused by haptens that combine with proteins (particularly the amino acid lysine) in the skin of some people to produce an immune response. Reactions to poison ivy (Figure 4), cosmetics, and the metals in jewelry (especially nickel) are familiar examples of these allergies.

Figure 5 The development of an allergy (allergic contact dennatitis) to catechols from the poison ivy plant. Pentadecacatechol is a mixture of catechols, which are oils secreted by the plant thatdissolve easily in skin oils and penetrate the skin. In theskin, the catechols function as haptens - that is, theycombine with skin proteins to become antigenic andprovoke an immune response. The first contact withpoison ivy sensitizes the susceptible person, andsubsequent exposure results in contact dermatitis.

Figure 1c. A schematic view of cellular reactions during the type I allergic response. (a) Sensitization (initial contact with sensitizing dose). (b) Provocation (later contacts with provocative dose).

Figure 1d. The spectrum of reactions to inflammatory cytokines and the common symptoms they elicit in target tissues and organs. Note the extensive overlapping effects.

Figure 1e Immunotherapy for IgE Allergies (a) Repeated injections of very small amounts of antigenare given over several months. (b) This regimen leads tothe formation of specific IgG antibodies. The IgG reactswith antigen before it can bind to IgE, and therefore itblocks the IgE reaction.

5. The immune diseases we have covered so far are all caused by foreign antigens. In the case of autoimmunity, individuals actually develop hypersensitivity to their own cells. This pathologic process accounts for autoimmune diseases, in which autoantibodies, T cells, and in some cases, both, mount an abnormal attack against self antigens. The scope of autoimmune diseases is extremely varied. In general, they are either systemic, involving several major organs, or organ-specific, involving only one organ or tissue. They usually fall into the categories of type II or type III hypersensitivity, depending upon how the autoantibodies bring about injury. Some major autoimmune diseases, their targets, and basic pathology are presented in table 1.

Table 1

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