Ferritin in autoimmune diseases

Gisele Zandman-Goddard, Yehuda Shoenfeld*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

Abstract

Iron, an essential element for many important cellular functions in all living organisms, can catalyze the formation of potentially toxic free radicals. Excessive iron is sequestered by ferritin in a nontoxic and readily available form in a cell. Ferritin is composed of 24 subunits of different proportions of two functionally distinct subunits: ferritin H and L. The expression of ferritin is under delicate control and is regulated at both the transcriptional and post-transcriptional levels by iron, cytokines, hormones, and oxidative stress. Mutations in the ferritin gene cause the hereditary hyperferritinemia-cataract syndrome and neuroferritinopathy. Hyperferritinemia is associated with inflammation, infections, and malignancies. While elevated levels of ferritin are characteristic of adult-onset Still's disease and hemophagocytic syndrome, both associated with inflammation, it has scantly been evaluated in other autoimmune diseases. In this review, we describe ferritin structure and function, hyperferritinemia in disease states and in autoimmune diseases.

Original languageEnglish
Pages (from-to)457-463
Number of pages7
JournalAutoimmunity Reviews
Volume6
Issue number7
DOIs
StatePublished - Aug 2007
Externally publishedYes

Keywords

  • Dermatomyositis
  • Ferritin
  • Multiple sclerosis
  • Polymyositis
  • Rheumatoid arthritis
  • Systemic lupus erythematosus
  • Thyroiditis

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