Pathogenesis of Immune Complex Mediated Diseases

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Antigen-antibody complexes are produced during normal immune responses, but they cause disease only when they are produced in excessive amounts, are not efficiently cleared, and become deposited in tissues. The amount of immune complex deposition in tissues is determined by the nature of the complexes and the characteristics of the blood vessels. Small complexes are often not phagocytosed and tend to be deposited in vessels more than large complexes, which are usually cleared by phagocytes. Complexes containing cationic antigens bind avidly to negatively charged components of the basement membranes of blood vessels and kidney glomeruli. Such complexes typically produce severe and long-lasting tissue injury. Capillaries in the renal glomeruli and synovia are vessels in which plasma is ultrafiltered (to form urine and synovial fluid, respectively) by passing through the capillary wall at high hydrostatic pressure, and these locations are among the most common sites of immune complex deposition. However, immune complexes may be deposited in small vessels in virtually any tissue. Immune complexes may also bind to Fc receptors of mast cells and leukocytes and activate these cells to secrete cytokines and vasoactive mediators. These mediators may cause more immune complex deposition in vessel walls by increasing vascular permeability and blood flow.

The deposition of immune complexes in vessel walls leads to complement- and Fc receptor-mediated inflammation and injury to the vessels and adjacent tissues. Deposits of antibody and complement may be detected in the vessels, and if the antigen is known, it is possible to identify antigen molecules in the deposits as well (see Fig. 18-3B).

Many systemic immunologic diseases in humans are caused by the deposition of immune complexes in blood vessels. Some common examples of autoimmune immune complex diseases are systemic lupus erythematosus (SLE), in which the complexes consist of nuclear antigens and antibodies, and several forms of nephritis and vasculitis (Table 18-3). In almost 50% of cases of one type of immune complex-mediated vasculitis involving medium-size muscular arteries, called polyarteritis nodosa, the complexes are made up of viral antigen and antibodies, and the disease is a late complication of viral infection, most often with hepatitis B virus. This also is the mechanism of a disease called poststreptococcal glomerulonephritis that develops in rare cases after streptococcal infection and is caused by complexes of streptococcal antigen and antibodies depositing in the glomeruli of the kidney.

TABLE 18-3 Examples of Human Immune Complex-Mediated Diseases

Disease

Antigen Involved

Clinicopathologic Manifestations

Systemic lupus erythematosus

DNA, nucleoproteins, others

Nephritis, arthritis, vasculitis

Polyarteritis nodosa

Hepatitis B virus surface antigen

Vasculitis

Poststreptococcal glomerulonephritis

Streptococcal cell wall antigens; may be "planted" in glomerular basement membrane

Nephritis

Serum sickness

Various proteins

Arthritis, vasculitis, nephritis

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