It
appears that heart disease will turn out to be an autoimmune system
failure that misidentifies a a ordinary protein as foreign. Thus the
idea that it can be treated with vaccine is creditable. This also
explains why my little experiment that I conducted for three years
applying tetracycline appeared to reduce low level inflammation.
It
also suggests that allergies may be linked to all this.
Thus
we possibly have a new strategy that will be jumped on pretty quickly
that may also resolve allergies. This is very good news as there are
no convincing protocols out there to prevent the disease at all.
Most recommendations are thinly disguised efforts to blame the
patient.
Researchers at the La
Jolla Institute for Allergy & Immunology have identified the
specific type of immune cells (CD4 T cells) that orchestrate the
inflammatory attack on the artery wall, which is a major
contributor to plaque buildup in heart disease. (Credit: Image
courtesy of La Jolla Institute for Allergy and Immunology)
ScienceDaily (Aug. 14,
2012) — Most people probably know that heart disease remains
the nation's No. 1 killer. But what many may be surprised to learn is
that cholesterol has a major accomplice in causing dangerous arterial
plaque buildup that can trigger a heart attack. The culprit?
Inflammatory cells produced by the immune system.
A number of research
studies have demonstrated inflammation's role in fueling plaque
buildup, also known as atherosclerosis, which is the underlying cause
of most heart attacks and strokes, but knowledge of which immune
cells are key to this process has been limited -- until now.
Researchers at the La
Jolla Institute for Allergy & Immunology have identified the
specific type of immune cells (CD4 T cells) that orchestrate the
inflammatory attack on the artery wall. Further, the researchers
discovered that these immune cells behave as if they have previously
seen the antigen that causes them to launch the attack. "The
thing that excites me most about this finding is that these immune
cells appear to have 'memory' of the molecule brought forth by the
antigen-presenting cells," said Klaus Ley, M.D., an expert in
vascular immunology, who led the study in mouse models. "Immune
memory is the underlying basis of successful vaccines. This means
that conceptually it becomes possible to consider the development of
a vaccine for heart disease."
Dr. Ley said he
believes the antigen involved is actually a normal protein that
the body mistakes as being foreign and therefore launches an immune
attack resulting in inflammation in the arteries. "Essentially,
we're saying that there appears to be a strong autoimmune component
in heart disease," he said, explaining that autoimmune
diseases result from the body's mistaken attack on normal cells.
"Consequently, we could explore creating a "tolerogenic"
vaccine, such as those now being explored in diabetes, which could
induce tolerance by the body of this self-protein to stop the
inflammatory attack."
The study was
published online August 13 in the Journal of Clinical
Investigation.
Dr. Ley cautions that
creating a vaccine is a complex process that could take years to
develop. However it offers exciting potential. "If successful, a
tolerogenic vaccine could stop the inflammation component of heart
disease," he said. "This could probably be used in
conjunction with the statins (cholesterol-lowering drugs) that have
already taken a significant chunk out of the numbers of people with
heart disease. Together, they could deliver a nice one-two punch that
could be important in further reducing heart disease."
Dr. Ley said
antigen-presenting cells take up infectious organisms, foreign
materials and self-proteins (in the case of autoimmune diseases) and
"chop them into little pieces called epitopes" and then
display the pieces on the surface of the cell. "The T cell comes
along, and if it has the correct receptors, it will recognize the
epitope pieces and make cytokines (a type of immune system soldier
molecule) that attack the material and cause inflammation."
Autoimmune diseases include such illnesses as type 1 diabetes,
rheumatoid arthritis and multiple sclerosis.
In the study, Dr. Ley
and his team used live cell imaging techniques to track immune cells
in normal and artherosclerotic mouse aortas. He said in mice with
atherosclerosis, there are a large number of antigen-experienced T
cells that have already seen certain epitope pieces (from self
proteins) that they perceive as foreign. "The T cells talk to
the antigen-presenting cells and, in response, make cytokines that
launch an attack. This is what makes the inflammation in the vessel
wall persistent." Inflammatory cells join fat and cholesterol
to form artery-clogging plaque that can eventually block blood flow,
leading to a heart attack.
"It wasn't
previously known that antigen-experienced T cells existed in the
vessel wall," said Dr. Ley. "This experiment makes me
now believe that it may be possible to build a vaccine for heart
disease."
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