Chapter 3

Diseases of the immune system take many forms, including hypersensitivity reactions, autoimmune disorders, and immunodeficiency states. Hypersensitivity reactions occur as one of four types (types I–IV). Autoimmune diseases are the result of a failure in the immune system to recognize self-antigens, resulting in production of antibodies that react against normal components of cells. Most of the autoimmune diseases are associated with one or more specific antibodies, which can be identified by laboratory tests to aid in diagnosis. Immunodeficiency states can be hereditary or acquired. A major cause of acquired immunodeficiency is human immunodeficiency virus (HIV) infection. The concepts of immunity are also important in regard to transplantation efforts. This chapter will discuss hypersensitivity reactions, transplantation pathology, autoimmune diseases, amyloidosis, and both hereditary and acquired immunodeficiency.

Overview: There are four types of hypersensitivity reactions, each of which has a different mechanism. These four types of hypersensitivity reactions will be discussed below.

### Type I Hypersensitivity Reaction

Mechanism: Exposure to an antigen results in the formation of IgE. The antigen reacts with CD4+ cells, which differentiate to TH2 cells. TH2 cells release interleukin-3 (IL-3), IL-4, and IL-5. IL-5 stimulates eosinophils, and IL-4 activates IgE-producing B cells. The IgE binds to mast cells. Subsequent exposure to the same antigen results in binding of the antigen to IgE bound to mast cells, with the consequence of degranulation of the mast cells and release of mediators (e.g., histamine). The release of mediators causes increased vascular permeability, leading to edema and increased smooth muscle contraction and eventually to bronchoconstriction.

Sequence of events in type I hypersensitivity reaction

1. Early phase (occurs within 5–30 minutes of exposure to antigen): Characterized by vasodilation, increased vascular permeability, and increased smooth muscle contraction. The early phase is due to binding of antigen to IgE bound to mast cells, with subsequent degranulation of the mast cells and release of mediators.

2. Late phase (occurs after 2–24 hours and lasts for days): Characterized by infiltration by neutrophils, eosinophils, basophils, and monocytes, and results in mucosal damage due to release of mediators by these recruited inflammatory cells.

Forms of type I hypersensitivity reactions

• Systemic anaphylaxis: Due to parenteral administration of antigen; for example, a bee sting or a reaction to penicillin.
• Local reaction: Urticaria (hives).

Causes: Penicillin, angiotensin-converting enzyme (ACE) inhibitors, intravenous (IV) contrast and other drugs, proteins (e.g., insect venoms), and food.

Clinical presentation of type I hypersensitivity reaction: Symptoms and signs include abrupt onset (within 30 minutes of exposure to antigen) of rash, nausea and vomiting and facial swelling, wheezing and stridor, and hypotension and tachycardia. Serum tryptase is a marker of anaphylaxis.

Complications of systemic anaphylaxis: Death due to airway compromise from laryngeal edema.

### Type II Hypersensitivity Reaction

Overview of general mechanism: Antibodies directed against target antigens ...

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