Role of Genetic Factors in Drug-Related Autoimmunity

Adams, Louis E.; Mongey, Anne‐Barbara

doi:10.1177/096120339400300603

Cited by 18 publications

(12 citation statements)

References 51 publications

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“…Chemical/physical factors Many drugs such as procainamide and hydralazine, which are aromatic amines or hydrazines, can induce a lupus-like syndrome, especially in individuals who are genetically slow acetylators. 134 Both aromatic amines and hydrazines, and their derivatives, can be found in a wide variety of compounds used in agriculture and industry, and commercial applications. Hydrazine itself also occurs naturally in tobacco and tobacco smoke.…”

Section: Environmental Triggersmentioning

confidence: 99%

Pathogenesis of systemic lupus erythematosus

Mok

Lau²

2003

Journal of Clinical Pathology

722

518

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Section: Environmental Triggersmentioning

confidence: 99%

Pathogenesis of systemic lupus erythematosus

Mok

Lau²

2003

Journal of Clinical Pathology

722

518

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“…A second line of evidence comes from studies on drug‐induced lupus. This autoimmune disease can be induced by more than 40 medications, such as the anti‐hypertensive drug hydrazine and the anti‐arrythmic drug procainamide, particularly in individuals who are genetically slow acetylators 59 . Interestingly, aromatic amines and hydrazine derivatives can be found in a wide variety of compounds used in agriculture, industry, and commercial applications.…”

Section: Epigenetic Factors Underlying Impaired B Cell Tolerancementioning

confidence: 99%

“…This autoimmune disease can be induced by more than 40 medications, such as the anti-hypertensive drug hydrazine and the antiarrythmic drug procainamide, particularly in individuals who are genetically slow acetylators. 59 Interestingly, aromatic amines and hydrazine derivatives can be found in a wide variety of compounds used in agriculture, industry, and commercial applications. Hydrazine itself also occurs in tobacco and tobacco smoke, and, as discussed below, a lupus-like syndrome has been reported in individuals who have been in contact with these agents.…”

Section: Epigenetic Factors Underlying Impaired B Cell Tolerancementioning

confidence: 99%

Epigenetics in lupus

Zouali

2011

Annals of the New York Academy of Sciences

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Accumulating epidemiological, clinical, and experimental evidence supports the conclusion of a critical role of epigenetic factors in immune programming. This understanding provides the basis for elucidating how the intricate interactions of the genome, epigenome, and transcriptome shape immune responses and maintain immune tolerance to self-antigens. Deciphering the precise contribution of epigenetic factors to autoimmunity, and in particular to lupus, has become an active research area. On one hand, it is well established that environmental factors have an impact on the epigenome and, therefore, on the transcriptional and translational machinery of specific cell types; on the other, the environment also plays an important role in the severity of lupus and other autoimmunity diseases. Determining how epigenetics "connects" the environment to cell biology and to autoreactivity will be key for advancing our understanding in this field and, possibly, for developing novel preventive strategies.

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“…4 The most popular theory linking autoimmunity to MS is that a triggering infection by an acute or "hit-and-run" virus induces molecular mimicry, a phenomenon of selfdirected immunity by microbial epitopes. 2 However, immune-mediated tissue damage can also result from viral infections in which the host immune response is directed to viral rather than self proteins, or as a consequence of nonspecific or bystander immune response that changes the local cytokine environment.…”

mentioning

confidence: 99%

A specific viral cause of multiple sclerosis: One virus, one disease

Lipton

Liang

Hertzler

et al. 2007

Annals of Neurology

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"Multiple sclerosis is an autoimmune disease," is heard so often that it is widely accepted as fact by the current generation of students and physicians. Yet, although it is undisputed that multiple sclerosis (MS) is immune mediated, an autoimmune mechanism remains unproven. Immune-mediated tissue damage can also result from viral infections in which the host immune response is directed to viral rather than self proteins, or as a consequence of nonspecific or bystander immune responses that change the local cytokine environment. Increasing evidence suggests that poorly controlled host immune responses account for much of the tissue damage in chronic infections, and it has been postulated that a similar mechanism may underlie many chronic diseases with features suggestive of an infectious causative factor, including MS. A recent study suggesting that oligodendrocyte death accompanied by microglial activation is the primary event in new MS lesion formation, rather than lymphocyte infiltration, could change the current mindset almost exclusively focused on autoimmunity. This review presents the rationale for considering MS a single disease caused by one virus, as well as the anticipated pattern of a persistent central nervous system infection, the application of Koch's postulates to viral discovery in MS as the causative agent, and tissue culture-independent genotypic approaches to viral discovery in MS.

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Role of Genetic Factors in Drug-Related Autoimmunity

Cited by 18 publications

References 51 publications

Pathogenesis of systemic lupus erythematosus

Pathogenesis of systemic lupus erythematosus

Epigenetics in lupus

A specific viral cause of multiple sclerosis: One virus, one disease

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