Viruses and Autoimmune Diseases

Oldstone, Michael B. A.

doi:10.1046/j.1365-3083.1997.d01-145.x

Cited by 15 publications

(7 citation statements)

References 48 publications

(107 reference statements)

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“…Oldstone [51] and others [52,53] have studied transgenic IMD mice models for autoimmune diseases to examine the molecules and events involved in virus-induced autoimmune diseases. Oldstone [51] used the rat insulin promoter to express a viral gene in the i cells of Langerhans.…”

Section: Viral Transgenesmentioning

confidence: 99%

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Current cases in which epitope mimicry is considered as a component cause of autoimmune disease: immune-mediated (type 1) diabetes

Kukreja¹,

Maclaren²

2000

CMLS, Cell. Mol. Life Sci.

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Autoimmune diseases result from a combination of genetic, immunologic, hormonal, and environmental factors. Infectious agents may induce the breakdown of immunological tolerance and the appearance of autoreactivity. However, the specific relationship between infection and autoimmunity is still unclear. One of the mechanisms responsible could be molecular mimicry between the infectious agent and self. The concept of molecular mimicry is a viable hypothesis in the investigation of the etiology, pathogenesis, treatment, and prevention of autoimmune disorders. Immune-mediated (type 1) diabetes in humans and in non-obese diabetic (NOD) mice is polygenic and characterized by autoimmune destruction of insulin-producing pancreatic beta cells in islets of Langerhans. In NOD mice, a T-helper 1 (Th1)-based autoimmune response arises spontaneously against glutamate decarboxylase (GAD) concurrently with the onset of insulitis. Subsequently. this Th1-type autoreactivity spreads intra- and intermolecularly to other beta cell autoantigens, suggesting that a Th1-type response is responsible for the progression of the disease, whereas Th2 responses when experimentally induced are protective. In humans, a homology between GAD and the P2-C protein of Coxsackie B make a cause-and-effect molecular mimicry an attractive hypothesis. Evidence to support the concept of molecular mimicry in diabetes is reviewed.

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Section: Viral Transgenesmentioning

confidence: 99%

“…Oldstone [51] used the rat insulin promoter to express a viral gene in the i cells of Langerhans. Diabetes did not occur spontaneously (in Table 1.…”

Section: Viral Transgenesmentioning

confidence: 99%

Current cases in which epitope mimicry is considered as a component cause of autoimmune disease: immune-mediated (type 1) diabetes

Kukreja¹,

Maclaren²

2000

CMLS, Cell. Mol. Life Sci.

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“…It has been hypothesised that infection with acute or persistent DNA and RNA viruses induce, accelerate or enhance autoimmune responses and cause autoimmune disease (reviewed in [261][262][263]). The mechanism might be that infectious agents activate lymphocytes that also respond to self-antigens [264][265][266].…”

Section: Viral Induction Of Autoimmune Diseasementioning

confidence: 99%

Apoptosis and autoimmune disease

O’Reilly¹,

Strasser²

1999

Inflamm. res.

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The process of programmed cell death or apoptosis was already noted in 1842 by Vogt [1], but it was not until the more recent studies of Kerr et al. 1972 [2] that an explosion of interest in apoptosis research occurred. Genetic, biochemical and cellular analysis in certain mammals, in the nematode Caenorhabditis elegans and in the fruitfly Drosophila melanogaster have identified several apoptosis regulating genes. This indicates that programmed cell death is an active, genetically controlled process. Many of the known cell death regulators are homologous in mammals, nematodes and insects, indicating that apoptosis is an evolutionarily conserved process. Apoptosis can be induced via multiple independent signalling pathways which converge upon a common final effector machinery. This stimulates activation of latent cysteine proteases (caspases), which cleave vital cellular substrates and thereby lead to the death of cells. The regulatory pathways of apoptosis are becoming clear with the discovery of specific signalling molecules. It has become evident that many disease processes including autoimmunity and cancer can be caused by deregulation of the apoptotic process. With the discovery of novel cell surface-bound death receptors, their ligands and further insight into the apoptotic machinery within the cell, research may ultimately lead to the design of therapies that allow intervention in the apoptotic process. The aims of such strategies would be to turn on apoptosis in neoplastic cells or in lymphocytes that are causing autoimmune disease or to prevent cell death in degenerative disorders. This review describes current understanding of the molecular regulation of apoptosis, and focuses on issues relating to possible roles of defective cell death control in autoimmunity.

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“…Interference with the cells of the immune system is a known mechanism by which viruses evade the host response and become chronically infective (Oldstone., 1997). Infection of extrahepatic tissues is supported by the finding that HCV quasispecies composition differs according to the sample type, i.e., liver, serum, or PBMCs (Cabot et al, 1997;Di Liberto et al, 2006;Fujii et al, 1996;Maggi et al, 1997;Navas et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

IRES complexity before IFN‐alpha treatment and evolution of the viral load at the early stage of treatment in peripheral blood mononuclear cells from chronic hepatitis C patients

Thélu

Leroy

Ramzan

et al. 2007

Journal of Medical Virology

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HAL is a multi-disciplinary open access archive for the deposit and dissemination of scientific research documents, whether they are published or not. The documents may come from teaching and research institutions in France or abroad, or from public or private research centers. L'archive ouverte pluridisciplinaire HAL, est destinée au dépôt et à la diffusion de documents scientifiques de niveau recherche, publiés ou non, émanant des établissements d'enseignement et de recherche français ou étrangers, des laboratoires publics ou privés.

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Viruses and Autoimmune Diseases

Cited by 15 publications

References 48 publications

Current cases in which epitope mimicry is considered as a component cause of autoimmune disease: immune-mediated (type 1) diabetes

Current cases in which epitope mimicry is considered as a component cause of autoimmune disease: immune-mediated (type 1) diabetes

Apoptosis and autoimmune disease

IRES complexity before IFN‐alpha treatment and evolution of the viral load at the early stage of treatment in peripheral blood mononuclear cells from chronic hepatitis C patients

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