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Chapter 2 : Principles of Molecular Mimicry and Autoimmune Disease

Author: Irun R. Cohen1
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Affiliations: 1: Irun R. Cohen Department of Immunology, The Weizmann Institute of Science, Rehovot, Israel 76100
Content Type: Monograph
Publication Year: 2000

Category: Microbial Genetics and Molecular Biology

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Abstract:

The role of molecular mimicry in the host-parasite relationship is complex, and different investigators may have different ideas in mind when they consider the subject. The aim is to examine the immunological principles behind the phenomenon of host-parasite mimicry and autoimmune disease. Antigen recognition, including self-recognition, requires pre-existing T cells and B cells that bear antigen receptors complementary to the antigen, be it a foreign antigen or a self-antigen; this is the basic tenet of the clonal selection theory of acquired immunity. So, an autoimmune disease would not be possible unless autoimmune lymphocytes preceded the outbreak of the disease. If rodents and humans feature immunological homunculi, then the positive selection of strong autoimmunity to at least some self-antigens has been conserved during evolution and so is likely to be advantageous. The classical formulation of the theory taught that immune specificity was achieved automatically. Macrophages, T cells, and B cells each sense a unique aspect of the immune encounter, and, at the same time, these cells mutually exchange information (by way of cytokines, chemokines, antibodies, and other cell interaction molecules) that is obtained from their different views. To induce an autoimmune disease, an infectious agent must activate physiological autoimmunity unnaturally. The potential for mimicry inherent in the evolution and coevolution of hosts and parasites is compounded by the intrinsic degeneracy of biological receptors.

Citation: Cohen I. 2000. Principles of Molecular Mimicry and Autoimmune Disease, p 17-26. In Cunningham M, Fujinami R (ed), Molecular Mimicry, Microbes, and Autoimmunity. ASM Press, Washington, DC. doi: 10.1128/9781555818074.ch2
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References

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