Abstract
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 language | English |
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Pages (from-to) | 168-175 |
Number of pages | 8 |
Journal | Nishinihon Journal of Urology |
Volume | 67 |
Issue number | 4 |
Publication status | Published - 2005 Apr 1 |
Externally published | Yes |
Keywords
- Autoimmune diseases
- Cytokine
- Dendritic cell
- Inflammation
- Signal transduction
- Tumorigenesiss
ASJC Scopus subject areas
- Urology