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A20 edits ubiquitin and autoimmune paradigms

Nature Genetics volume 43, pages 822–823 (2011)Cite this article

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Complex autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus, type 1 diabetes, multiple sclerosis, psoriasis and inflammatory bowel disease have different pathological presentations but have overlapping genetic susceptibility variants. A new study using mice lacking Tnfaip3, whose ortholog is linked to autoimmune disease in humans, leads to insights in the role of one molecular driver of varied clinical symptomatology in disparate autoimmune disorders.

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Figure 1: A20 deficiency in specific cell types in mice leads to different phenotypes that suggest mechanisms of human autoimmune disease physiopathology.

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Authors and Affiliations

  1. Flavius Martin is in the Department of Immunology, Genentech, South San Francisco, California, USA.,

    Flavius Martin

  2. Vishva M. Dixit is in the Department of Physiological Chemistry, Genentech, South San Francisco, California, USA.,

    Vishva M Dixit

Authors
  1. Flavius Martin
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  2. Vishva M Dixit
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Corresponding authors

Correspondence to Flavius Martin or Vishva M Dixit.

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Competing interests

F.M. and V.M.D. are employees of Genentech, a member of the Roche group.

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Martin, F., Dixit, V. A20 edits ubiquitin and autoimmune paradigms. Nat Genet 43, 822–823 (2011). https://doi.org/10.1038/ng.916

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