Heavy Metals in Autoimmune Diseases: Too Much Noise in Autoimmunity

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

Abstract

The loss of the ability of the immune system to recognize “self” antigens, i.e. tolerance, mounts an immune response against one’s own tissues and cells, hence autoimmunity. The susceptibility to autoimmune diseases results from an interplay of several variables mainly genetic, environmental, and epigenetic factors. Specific triggers include both intrinsic and extrinsic factors. Of those factors, dietary factors, infections, smoking, stress, and toxic chemicals have been shown to influence disease etiopathogenesis. Heavy metals are naturally occurring elements with high atomic density. Their wide distribution stems from their widespread use in industry, medical, and technological fields. Heavy metals exert an important biochemical and physiological function in the human body. They are considered important constituents of several key enzymes and thus play an important role in oxidation-reduction reactions. Nevertheless, at high doses, heavy metals could have detrimental effects resulting in epigenetic modifications, reactive oxygen species production, activation of the innate and adaptive immune cells, and shifting the cytokine expression to proinflammatory profile. Current scientific evidence points toward the role of heavy metals in the exacerbation of various autoimmune diseases including systemic lupus erythematosus, rheumatoid arthritis, and multiple sclerosis. The purpose of this chapter is to closer inspect the clinical evidence regarding the role of heavy metals in the various aspects of autoimmune diseases.

Original languageEnglish
Title of host publicationAutoimmune Disorders
Subtitle of host publicationAdjuvants and Other Risk Factors in Pathogenesis
Publisherwiley
Pages201-223
Number of pages23
ISBN (Electronic)9781119858430
ISBN (Print)9781119858416
DOIs
StatePublished - 1 Jan 2024

Keywords

  • aluminum
  • autoimmune diseases
  • heavy metals
  • reactive oxygen species
  • rheumatoid arthritis

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