1. Desensitization or immunotherapy is often effective in decreasing the type I hypersensitivity state. (Figure 18.3)

2. A new treatment, using an engineered anti-IgE, is proving effective in treating asthma.

18.2 Type II Hypersensitivities: Cytotoxic (Table 18.1)

1. Type II hypersensitivity reactions, or cytotoxic reactions, are caused by antibodies that can destroy normal cells by complement lysis or by antibody-dependent cellular cytotoxicity (ADCC).

Transfusion Reactions (Table 18.2)

1. The ABO blood groups have been the major cause of transfusion reactions.

Review Questions 457

Hemolytic Disease of the Newborn (Figure 18.4)

1. The Rhesus blood groups are usually responsible for this disease.

18.3 Type III Hypersensitivities: Immune Complex-Mediated

1. Type III hypersensitivity reactions are mediated by small antigen-antibody complexes that activate complement and other inflammatory systems, attract neutrophils, and contribute to inflammation.

2. The small immune complexes are often deposited in small blood vessels in organs, where they cause inflammatory disease—for example, glomerulonephritis in the kidney or arthritis in the joints. (Figure 18.5, Table 18.3)

18.4 Type IV Hypersensitivities: Delayed Cell-Mediated

1. Delayed hypersensitivity reactions depend on the actions of sensitized T lymphocytes.

Tuberculin Skin Test (Figure 18.6)

1. A positive reaction to protein antigens of the tubercle bacillus introduced under the skin peaks 2 to 3 days after exposure to antigen.

Contact Hypersensitivities

1. Contact allergy, or contact dermatitis, occurs frequently in response to substances such as poison ivy, nickel in jewelry, and chromium salts in leather products. (Figures 18.7,18.8)

Delayed Hypersensitivity in Infectious Diseases

1. Delayed hypersensitivity is important in responses to many chronic, long-lasting infectious diseases.

18.5 Transplantation Immunity

1. Transplantation rejection of allografts is caused largely by type IV cellular reactions.

18.6 Autoimmune Diseases

1. Responses against substances of self can lead to autoimmune diseases. (Table 18.4)

The Spectrum of Autoimmune Reactions

1. Autoimmune diseases may be organ-specific or widespread.

2. Some autoimmune diseases are caused by antibodies produced to body components, and others by cell-mediated reactions.

Treatment of Autoimmune Diseases

1. Autoimmune diseases are usually treated with drugs that suppress the immune and/or inflammatory responses.

18.7 Immunodeficiency Disorders

1. Immunodeficiencies may be primary genetic or developmental defects in any components of the immune response, or they may be secondary and acquired. (Table 18.5)

Primary Immunodeficiencies (Table 18.6)

1. B-cell immunodeficiencies result in diseases involving a lack of antibody production, such as agammaglobulinemias and selective IgA deficiency.

2. T-cell deficiencies result in diseases such as DiGeorge syndrome.

3. Lack of both T- and B-cell functions results in combined immunodeficiencies, which may be severe.

4. Defective phagocytes are found in chronic granulomatous disease and Chediak-Higashi disease.

Secondary Immunodeficiencies

1. Acquired immunodeficiencies can result from malnutrition, immunosuppressive agents, infections (such as AIDS), and malignancies.

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