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Chapter 1 : An Overview: Molecular Mimicry and Disease

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Abstract:

This chapter discusses the microbe-host interactions by using several different microbe-host disease states to illustrate the importance and nature of the cross-reactions in the genetically programmed host. The concept of autoimmunity playing a role in this disease was introduced more than 50 years ago by a number of investigators when antibodies to the heart were noted in the sera of patients with acute rheumatic fever (ARF) and/or rheumatic heart disease. Turning to the cellular reactivity in patients with rheumatic fever (RF), lymphocytes from the RF valvular lesions have been an area of active investigation in the laboratory. For example, using a panel of monoclonal antibodies specific for various cell surface markers, researchers demonstrated that the valvular lesions contained equal numbers of macrophages and T cells. Helper T cells predominated in the more active cardiac lesions; the ratio of T helper cells to T suppressor cells in patients with chronic carditis closely resembled that seen in normal peripheral blood. The acute disease is the result of multiplication of the organism in the reticuloendothelial system followed by direct invasion of muscle tissue, the liver, and occasionally the meninges. As noted in a section on cross-reactivity, there appears to be a clear molecular association between structures of the HLA-B27 allele and antigens of . This is a clear case of molecular mimicry between host and microbes, and the sera of AS patients contain antibodies that are cross-reactive with both molecules.

Citation: Visvanathan K, Zabriskie J. 2000. An Overview: Molecular Mimicry and Disease, p 1-16. In Cunningham M, Fujinami R (ed), Molecular Mimicry, Microbes, and Autoimmunity. ASM Press, Washington, DC. doi: 10.1128/9781555818074.ch1

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Figure 1

Schematic representation of the various structures of the group A streptococcus. Note the wide variety of cross-reactions between its antigens and mammalian tissues.

Citation: Visvanathan K, Zabriskie J. 2000. An Overview: Molecular Mimicry and Disease, p 1-16. In Cunningham M, Fujinami R (ed), Molecular Mimicry, Microbes, and Autoimmunity. ASM Press, Washington, DC. doi: 10.1128/9781555818074.ch1
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Image of Figure 2
Figure 2

Schematic drawing of the two-dimensional structure of lipid A of gram-negative organisms and the peptidoglycan structure of gram-positive organisms. While there are obvious differences in their structures, the stenciled areas of each structure are quite similar.

Citation: Visvanathan K, Zabriskie J. 2000. An Overview: Molecular Mimicry and Disease, p 1-16. In Cunningham M, Fujinami R (ed), Molecular Mimicry, Microbes, and Autoimmunity. ASM Press, Washington, DC. doi: 10.1128/9781555818074.ch1
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Tables

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Table 1

A selection of cross-reactions between microbes and mammalian tissues

Citation: Visvanathan K, Zabriskie J. 2000. An Overview: Molecular Mimicry and Disease, p 1-16. In Cunningham M, Fujinami R (ed), Molecular Mimicry, Microbes, and Autoimmunity. ASM Press, Washington, DC. doi: 10.1128/9781555818074.ch1

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