Regulation of dendritic cell activation and autoimmunity by SOCS1

Toshikatsu Hanada, Akihiko Yoshimura

Research output: Contribution to journalArticlepeer-review


The suppressor of cytokine signaling-1 (SOCS1/JAB) negatively regulates not only the cytokine-signaling pathway, but also lipopolysaccharide (LPS)-induced macrophage activation. We found that SOCS1-deficient dendritic cells (DCs) were also hyperresponsive to interferon-γ (IFNγ) and interleukin-4 (IL-4). To define the role of SOCS1-deficient DCs in vivo, we generated mice in which the SOCS1 expression was restored in T and B cells under a SOCS1 -/- background. In these mice, DCs were accumulated in the thymus and spleen and produced high levels of BAFF/BLyS, resulting in the aberrant expansion of B cells and autoreactive antibody production. SOCS1-deficient DCs efficiently stimulated B cell proliferation in vitro and auto-antibody production in vivo. These results indicate that SOCS1 plays an essential role in the normal DC functions and in the suppression of systemic autoimmunity.

Original languageEnglish
Pages (from-to)168-175
Number of pages8
JournalNishinihon Journal of Urology
Issue number4
Publication statusPublished - 2005 Apr 1
Externally publishedYes


  • Autoimmune diseases
  • Cytokine
  • Dendritic cell
  • Inflammation
  • Signal transduction
  • Tumorigenesiss

ASJC Scopus subject areas

  • Urology


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