[articles] Journal of Autoimmunity

[Guest guest]

Some abstracts from:

Journal of Autoimmunity

Vol. 16, No. 3, May 2001

http://www.idealibrary.com/links/doi/10.1006/jaut.2000.0491

Epidemiology of Autoimmune Reactions Induced by

Vaccination

T. Chen, Pless, 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

T. Robles, 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

Sheri Nakken, R.N., MA, Hahnemannian Homeopath

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