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autoimmune treatments by antibiotics please read our e-book.
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What are autoantibodies?
What are they?
Autoantibodies are a group of antibodies
(immune proteins) that mistakenly target
and damage specific tissues or organs of
the body. One or more autoantibodies may
be produced by a person’s immune system
when it fails to distinguish between
“self” and “non-self" proteins. Usually
the immune system is able to
discriminate by recognizing foreign
substances (“non-self”) and ignoring the
body’s own cells ("self"), yet not
overreact to non-threatening substances
such as foods, dust and pollen, or
beneficial microorganisms. It creates
antibodies only when it perceives what
it has been exposed to as a threat
("non-self"). When the immune system
ceases to recognize one or more of the
body’s normal constituents as “self”, it
may produce autoantibodies that attack
its own cells, tissues, and/or organs,
causing inflammation and damage. The
causes of this inappropriate action are
varied and are not well understood,
often resulting in a chronic autoimmune
disorder. While there is not a direct
link, it is thought that many cases of
autoantibody production are due to a
genetic predisposition combined with an
environmental trigger (such as a viral
illness or a prolonged exposure to
certain toxic chemicals). Some families
have been shown to have a high
prevalence of autoimmune conditions;
however, individual family members may
have different autoimmune disorders or
may never develop an autoimmune
condition. Researchers believe that
there may also be a hormonal component
to the cause as many of the autoimmune
conditions are more common in women of
childbearing age.
The type of autoimmune disorder or
disease that occurs and the amount of
destruction done to the body depends on
which systems or organs are targeted by
the autoantibodies. Disorders caused by
autoantibodies that primarily affect a
single organ, such as the thyroid in
Graves’ disease or Hashimoto’s
thyroiditis, are often the easiest to
diagnose as they frequently present with
organ-related symptoms.
Disorders due to systemic autoantibodies
(affects multiple organs or systems) can
be much more elusive. Although the
associated autoimmune disorders are
rare, the signs and symptoms they cause
are relatively common and may include:
arthritis-type joint pain, fatigue,
fever, rashes, cold or allergy-type
symptoms, weight loss, and muscular
weakness. Additional complications may
include vasculitis (inflammation of
blood vessels) and anemia. Signs and
symptoms will vary from person to
person. They can vary over time and/or
with organ involvement, often tapering
off and then flaring up unexpectedly. To
complicate the situation, some may have
more than one autoantibody, have more
than one autoimmune disorder, and/or
have an autoimmune disorder without a
detectable level of an autoantibody.
This may make it difficult for the
doctor to identify the prime cause and
arrive at a diagnosis.
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The role of apoptosis in autoimmune
thyroid disorders and thyroid cancer
Jen-Der Lin,
professor of internal medicine.
Division of Endocrinology and Metabolism,
Department of Internal Medicine, Chang Gung
Memorial Hospital, Chang Gung University,
5 Fu-Shin Street, Kweishan County, Taoyuan
Hsien, Taiwan, Republic of China
Apoptosis, or programmed cell death, is
an active process of self destruction that
requires the activation of a genetic
programme that may lead to
changes in cell morphology, DNA
fragmentation, and protein cross
linking
Apoptosis can be triggered in several
ways and involves many cellular
functions. The
mechanism provides protection
from the possible consequences of
uncontrolled cell proliferation,
which could lead to neoplasia. Cell death is
a factor in the pathogenesis of
several diseases, including autoimmune
disorders, cancer, AIDS, and
neurodegenerative diseases. Regulation
of apoptosis in cells undergoing
proliferation may be the key to
reversing the natural progression of these
disorders.
Apoptosis involves the sequential
activation of a series of caspases, which
are proteolytic enzymes that degrade a
number of death substrates.
Caspase is activated by two pathways the
mitochondrial pathway and the
death receptor pathway and
thereby may trigger nuclear
enzymes to degrade chromosomal DNA and alter
mitochondrial function. Specific
pathways and non-specific signals (such as
cytotoxic drugs and radiation)
may activate caspase. The most common of
these pathways involves death
receptors that have structures belonging
to the tumour necrosis factor (TNF)
receptor superfamily of proteins.
Interaction of tumour necrosis factor with
this receptor can induce cell
death by the activation of various kinase
enzymes that act as secondary
messengers within the cell,
Another member of this family,
Fas antigen, and its ligand (FasL), are
molecules used by immune effector
cells to kill targets.
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