Page 568 - Review of Medical Microbiology and Immunology ( PDFDrive )

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Hypersensitivity (Allergy) 65
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CHAPTER C ONTENT S

Introduction
Immune Complex Diseases
Type I: Immediate (Anaphylactic) Hypersensitivity
Rheumatoid Arthritis
Atopy
Drug Hypersensitivity
Clinically Important Delayed Hypersensitivity Reactions
Desensitization
Practice Questions: USMLE & Course Examinations
Treatment & Prevention
Type II: Cytotoxic Hypersensitivity Self-Assessment Questions
Type III: Immune Complex Hypersensitivity
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Arthus Reaction
Serum Sickness

INTRODUCTION
The clinical manifestations of these reactions are typical
Hypersensitivity is the term used when an immune response
antigen to which the individual is hypersensitive. The first
results in exaggerated or inappropriate reactions harmful to
the host. Generally speaking, hypersensitivity reactions
induces the antibody), and subsequent contacts elicit the
occur in response to external stimuli (antigens) whereas
allergic response.
autoimmune reactions (see Chapter 66) occur in response to contact of the individual with the antigen sensitizes (i.e.,
Hypersensitivity reactions can be subdivided into four
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internal stimuli (antigens). The term allergy is often equated
main types. Types I, II, and III are antibody-mediated,
with hypersensitivity but more accurately should be limited
whereas type IV is cell-mediated (Table 65–1). Type I reac-
tions are mediated by IgE, whereas types II and III are
to the IgE–mediated reactions discussed later in the section
“Type I: Immediate (Anaphylactic) Hypersensitivity.”
TABLE 65–1 Immunologic Aspects of Hypersensitivity Reactions
Type
Cell Mediated
I (Immediate,
anaphylactic)
to the allergen again, the allergen cross-links the bound IgE on those cells. This causes
degranulation and release of mediators (e.g., histamine).
Antigens on a cell surface combine with IgG antibody. This leads to complement-mediated lysis
II (Cytotoxic) Antibody (IgE) Antigen (allergen) induces IgE antibody that binds to mast cells and basophils. When exposed
Antibody (IgG)
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of the cells (e.g., transfusion or Rh reactions) or autoimmune hemolytic anemia.
Antigen–antibody immune complexes are deposited in tissues, complement is activated, and
Antibody (IgG)
III (Immune complex)
polymorphonuclear cells are attracted to the site. They release lysosomal enzymes, causing
tissue damage.
IV (Delayed)
T lymphocytes activated/sensitized by an antigen release lymphokines upon second contact
with the same antigen. The lymphokines induce inflammation and activate macrophages,
which, in turn, release various inflammatory mediators.
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