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exotoxins 257 experimental autoimmune oophoritis
buttressed on both ends by introns, which are noncoding
regions of DNA. The coding sequence is transcribed in
mature mRNA and subsequently translated into proteins.
Exons produce folding regions, functional regions,
domains, and subdomains. Introns, which are junk DNA,
are spliced out. They constitute the turns or edges of secondary
structures.
exotoxins
An extracellular product of pathogenic microorganisms.
Exotoxins are 3- to 500-kDa polypeptides produced by
such microorganisms as Corynebacterium diphtheria,
Clostridium tetani, and C. botulinum. Vibrio cholerae
produces exotoxins that elevate cyclic adenosine monophosphate
(cAMP) levels in intestinal mucosa cells and
increase the flow of water and ions into the intestinal
lumen, producing diarrhea. Exotoxins are polypeptides
released from bacterial cells and are diffusible, thermolabile,
and able to be converted to toxoids that are
immunogenic but not toxic. Bacterial exotoxins are either
cytolytic, acting on cell membranes, or bipartite (A–B toxins),
linking to a cell surface through the B segment of the
toxin and releasing the A segment only after the molecule
reaches the cytoplasm, where it produces injury. Some
may serve as superantigens.
experimental allergic encephalomyelitis
An autoimmune disease induced by immunization of
experimental animals with preparations of brain or spinal
cord incorporated into Freund’s complete adjuvant. After
10 to 12 days, perivascular accumulations of lymphocytes
and mononuclear phagocytes surround the vasculature of
the brain and spinal cord white matter. Demyelination may
also be present, worsening as the disease becomes chronic.
The animals often develop paralysis. The disease can be
passively transferred from a sick animal to a healthy one of
the same strain with T lymphocytes, but not with antibodies.
The mechanism involves T cell receptor interaction
with an 18-kDa myelin basic protein molecule, which is an
organ-specific antigen of nervous system tissue. The CD4 +
T lymphocyte represents the phenotype that is reactive
with myelin basic protein. The immune reaction induces
myelinolysis, wasting, and paralysis. Peptides derived from
myelin basic protein (MBP) may be used to induce experimental
allergic encephalomyelitis in animals. This experimental
autoimmune disease is an animal model for multiple
sclerosis and postvaccination encephalitis in humans.
experimental allergic neuritis
An experimental disease induced by injecting rats with
peripheral nerve incorporated into Freund’s complete adjuvant.
P2 antigen is involved. Lymphocytes and macrophages
infiltrate the sciatic nerve, and paralysis may develop.
experimental allergic orchitis
An experimental autoimmune disease induced by injecting
experimental animals with isogeneic or allogeneic testicular
tissue incorporated into Freund’s complete adjuvant.
experimental allergic thyroiditis
An autoimmune disease produced by injecting experimental
animals with thyroid tissue or extract or thyroglobulin
incorporated into Freund’s complete adjuvant. It represents
an animal model of Hashimoto’s thyroiditis in humans, with
mixed extensive lymphocytic infiltrate. Another animal
model is the spontaneous occurrence of this disease in the
obese strain of chickens as well as in Buffalo rats.
Experimental allergic thyroiditis (EAT).
experimental autoimmune encephalymyelitis
Autoimmune demyelinating central nervous system disease
in animal models induced by immunizing rats with myelin
basic protein from the myelin sheath of nerves, incorporated
into Freund’s adjuvant. CD4 + T lymphocytes with
specificity for myelin sheath proteins secrete cytokines that
mediate the disease.
experimental autoimmune myasthenia gravis (EAMG)
Myasthenia gravis (MG) is an autoantibody-mediated
autoimmune disease. Experimental forms of MG were
made possible through the ready availability of AChR
from electric fish. Monoclonal antibodies were developed,
followed by molecular cloning techniques that permitted
definition of the AChR structure. EAMG can be induced in
more than one species of animals by immunizing them with
purified AChR from the electric ray (Torpedo californica).
The autoantigen, nicotinic AChR, is T cell-dependent. The
in vivo synthesis of anti-AChR antibodies requires helper T
cell activity. Antibodies specific for the nicotinic AChR of
skeletal muscle react with the postsynaptic membrane at the
neuromuscular junction.
experimental autoimmune myocarditis (EAM)
Murine model of human autoimmune myocarditis. Infection
of A/J and BALB/c mice with coxsackie Bc virus or immunization
of susceptible mice with cardiac myosin may lead
to development of EAM.
experimental autoimmune neuritis (EAN)
A condition induced in mammalian species by immunization
with peripheral nervous system (PNS) myelin, purified
PNS myelin proteins, or synthetic peptides of PNS antigens,
myelin basic protein, the PO glycoprotein, and the P2
protein. EAN develops 10 to 14 days after immunization
with ascending paraparesis and paralysis. CD4 + T cells
and macrophages infiltrate PNS tissue. Macrophages cause
demyelination. Autoantibodies to myelin may also play a
role in EAN pathogenesis.
experimental autoimmune oophoritis
Ovarian autoimmune disease induced by immunization
with synthetic peptides of mouse CP3, a glycoprotein with
sperm receptor activity located in the zona pellucida of
developing and mature oocytes. A single subcutaneous
injection of ZP3 peptide incorporated into Freund’s complete
adjuvant can induce the disease in (C57B1/6 × A/J)S 1
hybrid mice. It is marked by ovarian inflammation that may
be followed by ovarian follicle loss and ovarian atrophy.
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