V

Antibody

Antigen in excess

(b) Formation of immune complexes with slight antigen excess.

(b) Formation of immune complexes with slight antigen excess.

Complement activated

Endothelial cells of blood vessel

Endothelial cells of blood vessel

Complement in the blood

Spaces created by dilation of blood vessel

Basophil Mediators

Complement is activated by the immune complexes via the classical pathway. This causes basophils to degranulate, releasing mediators that increase vascular permeability (scale greatly exaggerated for clarity).

Complement in the blood

Spaces created by dilation of blood vessel

Basophil Mediators

Complement is activated by the immune complexes via the classical pathway. This causes basophils to degranulate, releasing mediators that increase vascular permeability (scale greatly exaggerated for clarity).

Basement membrane

Clump of immune complexes

Clump of immune complexes

Damaged cells Enzymes

(e) Activated complement attracts neutrophils and causes them to degranulate.

(f) Neutrophils release enzymes responsible for much of the tissue damage.

Damaged cells Enzymes

(d) Complexes circulate and are trapped in the basement membrane of small blood vessels.

(e) Activated complement attracts neutrophils and causes them to degranulate.

(f) Neutrophils release enzymes responsible for much of the tissue damage.

Figure 18.5 Type III Hypersensitivity: Immune Complex-Mediated

Nester-Anderson-Roberts: I III. Microorganisms and I 18. Immunologic Disorders I I © The McGraw-Hill

Microbiology, A Human Humans Companies, 2003

Perspective, Fourth Edition

18.4 Type IV Hypersensitivities: Delayed Cell-Mediated

Table 18.3 Pathogenesis of Immune Complex Disease

1. Antibody combines with excess soluble antigen.

2. The antibody-antigen combination reacts with complement.

3. Complexes are deposited in sites such as skin, kidney, and joints.

4. Fragments of complement cause release of histamine and other mediator substances from mast cells or basophils and also attract neutrophils.

5. Release of the mediators causes increased permeability of blood vessel walls.

6. Immune complexes penetrate or form in blood vessel walls.

7. Neutrophils enter the vessel walls chemotactically.

8. Neutrophils release lysosomal enzymes, especially proteases, that induce tissue injury.

Immune complex formation is also responsible for the localized injury or death of tissue, known as the Arthus reaction, that occurs if antigen is injected into the tissue of a previously immunized animal or person with high levels of circulating specific antibody. The immune complexes formed locally activate complement, producing complement components that attract neutrophils. The release of neutrophil contents and inflammation results in a local reaction that peaks at about 6 to 12 hours.

Serum sickness is an immune complex disease caused by passive immunization where an antibody-containing serum from a horse or other animal is injected into humans to prevent or treat a disease such as diphtheria or tetanus. The recipient of the animal serum may make an immune response to antigens in the foreign serum, and after 7 to 10 days enough immune complexes form to cause signs of disease, which include fever, inflammation of blood vessels, arthritis, and kidney damage. The disease generally resolves as the antigens of the animal serum are cleared. Of course, horses are no longer used to produce antibodies against diphtheria and tetanus; instead, hyperimmune human sera are used. The serum sickness form of hypersensitivity is rarely seen now, but it can occur following treatment of heart attack patients with the bacterial enzyme streptokinase to dissolve clots, after the use of serum from horses immunized with snake venom to treat snakebites in people, or in a few other rare instances. ■ passive immunity, p. 420

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