Introduction: Epitope mimicry as a component cause of autoimmune disease

Davies, J. M. (2000) Introduction: Epitope mimicry as a component cause of autoimmune disease. Cellular and Molecular Life Sciences, 57(4), pp. 523-526.

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The causes of autoimmune diseases have yet to be fully elucidated. Autoantibodies, autoreactive T cell responses, the presence of a predisposing major histocompatibility complex (MHC) haplotype and responsiveness to corticosteroids are features, and some are possibly contributory causes of autoimmune disease. The most challenging question is how autoimmune diseases are triggered. Molecular mimicry of host cell determinants by epitopes of infectious agents with ensuing cross-reactivity is one of the most popular yet still controversial theories for the initiation of autoimmune diseases [1]. Throughout the 1990s, hundreds of research articles focusing to various extents on epitope mimicry, as it is more accurately described in an immunological context, were published annually. Many of these articles presented data that were consistent with the hypothesis of mimicry but that did not actually prove the theory. Other equally convincing reports indicated that epitope mimicry was not the cause of the autoimmune disease despite sequence similarity between molecules of infectious agents and the host.

Some 20 years ago, Rothman [2] proposed a model for disease causation and I have used this as a framework to examine the role of epitope mimicry in the development of autoimmune disease. The thesis of Rothman’s model is that an effect, in this instance autoimmune disease, arises as a result of a cause. In most cases, multiple-component causes contribute synergistically to yield the effect, and each of these components alone is insufficient as a cause. Logically, some component causes, such as the presence of a particular autoimmune response, are also necessary causes.

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ID Code: 87927
Item Type: Journal Article
Refereed: Yes
Additional Information: No file attached.
Keywords: epitope, autoimmune disease, autoimmunity, B lymphocyte, cross reaction, disease model, environmental factor, genetic predisposition, human, immunopathogenesis, molecular mimicry, nonhuman, review, rheumatoid arthritis, systemic lupus erythematosus, T lymphocyte activation, Animals, Autoantigens, Autoimmune Diseases, Disease Models, Animal, Environmental Exposure, Epitopes, B-Lymphocyte, Genetic Predisposition to Disease, Humans
DOI: 10.1007/PL00000713
ISSN: 1420-682X
Divisions: Current > Schools > School of Biomedical Sciences
Current > QUT Faculties and Divisions > Faculty of Health
Deposited On: 30 Sep 2015 23:45
Last Modified: 01 Oct 2015 00:51

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