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Molecular mimicry happens inside and outside our body.
The terror activity WITHIN OUR BODY is Molecular mimicry!
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Molecular
mimicry
has
been
proposed
as a
pathogenetic
mechanism
for
autoimmune
disease,
as
well
as a
probe
useful
in
uncovering
its
etiologic
agents.
The
hypothesis
is
based
in
part
on
the
abundant
epidemiological,
clinical,
and
experimental
evidence
of
an
association
of
infectious
agents
with
autoimmune
disease
and
observed
cross-reactivity
of
immune
reagents
with
host
'self'
antigens
and
microbial
determinants.
For
our
purpose,
molecular
mimicry
is
defined
as
similar
structures
shared
by
molecules
from
dissimilar
genes
or
by
their
protein
products.
Either
the
molecules'
linear
amino
acid
sequences
or
their
conformational
fits
may
be
shared,
even
though
their
origins
are
as
separate
as,
for
example,
a
virus
and
a
normal
host
self
determinant.
An
immune
response
against
the
determinant
shared
by
the
host
and
virus
can
evoke
a
tissue-specific
immune
response
that
is
presumably
capable
of
eliciting
cell
and
tissue
destruction.
The
probable
mechanism
is
generation
of
cytotoxic
cross-reactive
effector
lymphocytes
or
antibodies
that
recognize
specific
determinants
on
target
cells.
The
induction
of
cross-reactivity
does
not
require
a
replicating
agent,
and
immune-mediated
injury
can
occur
after
the
immunogen
has
been
removed
a
hit-and-run
event.
Hence,
the
viral
or
microbial
infection
that
initiates
the
autoimmune
phenomenon
may
not
be
present
by
the
time
overt
disease
develops.
By a
complementary
mechanism,
the
microbe
can
induce
cellular
injury
and
release
self
antigens,
which
generate
immune
responses
that
cross-react
with
additional
but
genetically
distinct
self
antigens.
In
both
scenarios,
analysis
of
the
T
cells
or
antibodies
specifically
engaged
in
the
autoimmune
response
and
disease
provides
a
fingerprint
for
uncovering
the
initiating
infectious
agent.
Read
CIDPUSA
e-book
to
understand
how
diseases
are
triggered
and
how
to
cure
them.
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CONTINUE TO PAGE 3 to read about the recommended
intake
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