Page 574 - Review of Medical Microbiology and Immunology ( PDFDrive )

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CHAPTER 65 Hypersensitivity (Allergy)
563

Antigen
+

RBC
IgG
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mebooksfree.com mebooksfree.com Antigen–antibody Immune complexes Neutrophils are mebooksfree.com mebooksfree.com
complexes form
attracted by C5a;
are deposited on
they release
blood vessel wall,
in blood
enzymes that
complement is
destroy the
activated, and C3a
endothelium and
and C5a are
released
red cells escape
from within the
blood vessels
FIGURE 65–3
Immune complex hypersensitivity. RBC, red blood cell.
IgA nephropathy is one of the most common forms of
immune complex glomerulonephritis worldwide. This dis-
Vasculitis is an inflammation of the walls of blood vessels,
ease is characterized by deposits of IgA on the glomeruli.
including large, medium, and small arteries and veins. Several
The cause is unknown; no infectious agent has been associ- Vasculitis
diseases that manifest with vasculitis are caused by immune
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ated with this disease. The course of the disease varies
complexes, such as polyarteritis nodosa, Henoch-Schönlein
widely. Some patients are asymptomatic, some have mild
purpura (IgA vasculitis), cryoglobulin-related vasculitis, and
symptoms, and others progress rapidly to kidney failure.
Diagnosis is made by doing renal biopsy and demonstrat-
An important example of a cryoglobulin-related vasculitis
ing IgA deposits by immunohistologic testing.
occurs in hepatitis C virus infection. In contrast, some dis-
eases, such as giant cell arteritis (GCA) are caused by T cells
infiltrating the arterial wall. The most common form of GCA
Rheumatoid Arthritis
is temporal arteritis that involves the temporal artery.
Rheumatoid arthritis is a chronic inflammatory autoim-
The symptoms and signs of vasculitis vary depending
mune disease of the joints seen commonly in young
women. It is a systemic disease involving not only the
weight loss, arthralgia, myalgia, and abdominal pain. Some
joints but other organs as well, most often the lung and
findings often associated with vasculitis are palpable pur-
pericardium. Serum and synovial fluid of patients contain on the organ affected. Nonspecific findings include fever,
pura and mononeuritis multiplex which often manifests as
“rheumatoid factor” (i.e., IgM and IgG antibodies that
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foot or wrist drop. A complete description of the diseases in
bind to the Fc fragment of normal human IgG). Deposits
which vasculitis occurs is beyond the scope of this book.
of immune complexes (containing the normal IgG and
rheumatoid factor) on synovial membranes and in blood
vessels activate complement and attract polymorphonu-
HYPERSENSITIVITY
clear cells, causing inflammation. Patients have high titers
of rheumatoid factor and low titers of complement in
Delayed hypersensitivity is a function of T lymphocytes,
serum especially during periods when their disease is most
not antibody (Figure 65–4). It can be transferred by immu-
active (see page 573).
nologically committed (sensitized) T cells, not by serum.
Systemic Lupus Erythematosus
contact with the antigen and often lasts for days).
In certain contact hypersensitivities, such as poison oak,
Systemic lupus erythematosus is a chronic inflammatory
the pruritic, vesicular skin rash is caused by CD8-positive
autoimmune disease that affects several organs, especially The response is “delayed” (i.e., it starts hours [or days] after
cytotoxic T cells that attack skin cells that display the plant
the skin of the face, the joints, and the kidneys. Antibodies
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oil as a foreign antigen. In the tuberculin skin test, the
are formed against DNA and other components of the
indurated skin rash is caused by CD4-positive helper
nucleus of cells. These antibodies form immune complexes
that activate complement. Complement activation pro-
site. Table 65–4 describes some of the important clinical
duces C5a, which attracts neutrophils that release enzymes,
aspects of delayed hypersensitivities.
thereby damaging tissue (see pages 544 and 573).
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