HYPERSENSITIVITY

Autoimmune • Antibodies are formed to red blood

Hemolytic cell antigens
• Often occurs in association with
Anemia other diseases such as
lymphoma, or can occur in
response to administration of
certain drugs such as penicillin
• Hemolysis of red blood cells results
in anemia characterized by
fatigue, dyspnea on exertion, and
pallor.
• Diagnosis is made by the findings of
decreased hematocrit (and
hemoglobin), destroyed red blood
cells on blood smear, and a
positive Coombs antiglobulin test
which detects the autoantibodies.
• Treatment is directed at the
underlying problem or removal of
the drug and may also include
steroids
 Type II Hypersensitivity – Antibody-dependent cell
mediated toxicity with activation of cytotoxic cells
(natural killer or NK cells)

Y
Autoantibody
NK

Fc
receptor

Perforin and
enzymes

Host Target cell

 Type II Hypersensitivity – autoantibodies stimulate
host target cell receptors and alter function

Y
Y

HOST TARGET
CELL

ACTIVATION OF
CELL WITH
RELEASE OF
CELLULAR
PRODUCTS
 • Autoantibodies (called thyroid stimulating
Graves immunoglobulins) bind to receptors in
the thyroid gland.
Disease • Stimulate the gland to grow and produce
more thyroid hormone, but are not
subject to the normal TSH/T4 negative
feedback loop.
• Hyperthyroidism results with the clinical
manifestations of weight loss, tremor,
heat intolerance, muscle weakness,
and menstrual irregularity.
• Autoantibodies also cause infiltrative
changes that swell the front of the
lower leg (pretibial myxedema) and
behind the eyeball causing it to
protrude from the socket
(exophthalmus) due to T cell-mediated
stimulation of fibroblasts.
• Diagnosis is confirmed by measuring
increased thyroid hormone and thyroid
stimulating immunoglobulins
• Treatment consists of thyroid ablation –
monoclonal AB are being studied
 Type III Hypersensitivity
• Disorders are characterized clinical courses that tends to wax and wane
over time. Exacerbations and remissions are common, although tissue
damage may eventually result in organ failure.


• Raynaud’s phenomenon is characterized by a constellation of symptoms

that may be the only sequelae of the disorder, or they may be the first
manifestations of several other diseases including systemic lupus
erythematosus, scleroderma, and thromboangiitis obliterans. Immune
complex deposition and resultant activation of complement and
neutrophils causes inflammation of the blood vessels, joints and kidneys.
The most common complaint is of severe pain, numbness, and
progressive ischemic discoloration of the digits (white to blue to red)
especially upon cold exposure or stress. Individuals with this syndrome
may also complain of arthralgias, lymphadenopathy, fevers, and
decreased urine output (renal dysfunction).


• Membranous Glomerulonephritis is a slowly progressive disease that can

occur in association with other disorders such as infections, cancers,
collagen vascular diseases, drugs, and toxins, but is most commonly
idiopathic. Immune complexes deposit along the glomerular basement
membrane and activate complement and neutrophils. Gradually
progressive proteinuria is followed by complete renal failure in
approximately 40% of individuals with this disorder. Diagnosis is made by
renal biopsy with staining for these immune complexes
A Closer look at
Type III
Mechanism
TYPE IV DELAYED HYPERSENSITIVITY
 Type IV Hypersensitivity
• Contact dermatitis results from
the alteration of host skin cell
antigens due to contact with
an environmental antigen
such as the catechols from
the poison ivy plant. One to
two days after contact with
the plant, sensitized
individuals will develop
vesicles on the skin with
erythema and itching,
followed by scaling. Contact
dermatitis is also common
after contact with other
substances including metals
such as nickel (often found in
inexpensive jewelry),
cosmetics, topical medicines,
and rubber products.