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Gadd45β and Gadd45γ are critical for regulating autoimmunity

Authors
Journal
Journal of Experimental Medicine
0022-1007
Publisher
The Rockefeller University Press
Publication Date
Volume
202
Issue
10
Identifiers
DOI: 10.1084/jem.20051359
Keywords
  • Article
Disciplines
  • Medicine

Abstract

The number of effector T cells is controlled by proliferation and programmed cell death. Loss of these controls on self-destructive effector T cells may precipitate autoimmunity. Here, we show that two members of the growth arrest and DNA damage-inducible (Gadd45) family, β and γ, are critical in the development of pathogenic effector T cells. CD4+ T cells lacking Gadd45β can rapidly expand and invade the central nervous system in response to myelin immunization, provoking an exacerbated and prolonged autoimmune encephalomyelitis in mice. Importantly, mice with compound deficiency in Gadd45β and Gadd45γ spontaneously developed signs of autoimmune lymphoproliferative syndrome and systemic lupus erythematosus. Our findings therefore identify the Gadd45β/Gadd45γ-mediated control of effector autoimmune lymphocytes as an attractive novel target for autoimmune disease therapy.

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