"Since AID (autoimmune diseases) occur in the absence
of immunizations, it
is unlikely that immunizations are a major cause of AID." Pray tell,
who do
they know who hasn't been vaccinated? Sandy
Some abstracts from:
Journal of Autoimmunity
Vol. 16, No. 3, May 2001
Susan (AVN list)
http://www.idealibrary.com/links/doi/10.1006/jaut.2000.0491
Epidemiology of Autoimmune Reactions Induced by
Vaccination
Robert T. Chen, Robert Pless, Frank Destefano
In order for vaccinations to `work', the immune system
must be stimulated. The concern that immunizations may
lead to the development of autoimmune disease (AID)
has been questioned. Since AID occur in the absence of
immunizations, it is unlikely that immunizations are a
major cause of AID. Epidemiological studies are
needed, however, to assess whether immunizations may
increase the risk in some susceptible individuals.
This paper discusses the evidence for and against
vaccination as a risk factor for AID. Evidence for
immunizations leading to AID come from several sources
including animal studies, single and multiple case
reports, and ecologic association. However more
rigorous investigation has failed to confirm most of
the allegations. Unfortunately the question remains
difficult to address because for most AIDs, there is
limited knowledge of the etiology, background
incidence and other risk factors for their
development. This information is necessary, in the
absence of experimental evidence derived from
controlled studies, for any sort of adequate causality
assessment using the limited data that are available.
Several illustrative examples are discussed to
highlight what is known and what remains to be
explored, and the type of epidemiological evidence
that would be required to better address the issues.
Examples include the possible association of
immunization and multiple sclerosis (and other
demyelinating diseases), type 1 diabetes mellitus,
Guillain-Barre Syndrome, idiopathic thrombocytopenic
purpura, and rheumatoid arthritis. Copyright 2001
Academic Press
http://www.idealibrary.com/links/doi/10.1006/jaut.2000.0478
Protective Role of Infections and Vaccinations on
Autoimmune Diseases
Jean-François Bach
Infectious agents may induce autoimmune disease
through several mechanisms, notably antigen mimicry
and inflammation of the target organ; conversely,
infections may protect from autoimmune diseases. This
paradoxical effect has been demonstrated for a number
of bacteria, viruses and parasites on a variety of
spontaneous or experimentally induced animal models of
autoimmune diseases (e.g. experimental allergic
encephalomyelitis, lupus mice, non-obese diabetic
mice). The mechanisms of the protection are still
ill-defined, and probably vary according to models.
Stimulation of immunoregulatory CD4 T cells has been
shown to play a central role in several major models.
The role of superantigens is also important, like that
of Toll-like receptors. Antigen competition is another
major mechanism, itself open to several
interpretations. Epidemiological data support a
protective role of infections on human allergic and
autoimmune diseases. These diseases are much more
common in countries with high socio-economic
development (typically Northern countries in Europe).
The reason for this cannot be fully explained by
genetic differences because migrating populations
develop these diseases with the same incidence of the
adoptive country rather than that of the country of
origin. It is interesting that the frequency of these
diseases has been increasing in developed countries
over the last 20 years but not in undeveloped ones.
Copyright 2001 Academic Press
http://www.idealibrary.com/links/doi/10.1006/jaut.2000.0483
Type 1A Diabetes Induced by Infection and Immunization
David T. Robles, George S. Eisenbarth
Type 1A diabetes is an immune mediated disorder that
results from progressive destruction of the islet
-cells in the setting of genetic susceptibility. Both
MHC and non-MHC genes contribute to disease with class
II HLA molecules major determinants of susceptibility
or protection. The presence of multiple anti-islet
autoantibodies is associated with a high risk of
disease progression, and the first anti-islet
autoantibodies may appear as early as the first year
of life. Congenital rubella is the only infection
clearly associated with the development of type 1A
diabetes. With the ability to detect children in the
first year of life activating autoimmunity,
prospective studies may in the future document
additional environmental factors either increasing or
decreasing diabetes risk. Copyright 2001 Academic
Press
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