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 |
|---|---|
| Pages (from-to) | 168-175 |
| Number of pages | 8 |
| Journal | Nishinihon Journal of Urology |
| Volume | 67 |
| Issue number | 4 |
| Publication status | Published - 2005 Apr |
| Externally published | Yes |
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Keywords
- Autoimmune diseases
- Cytokine
- Dendritic cell
- Inflammation
- Signal transduction
- Tumorigenesiss
ASJC Scopus subject areas
- Urology
Cite this
Regulation of dendritic cell activation and autoimmunity by SOCS1. / Hanada, Toshikatsu; Yoshimura, Akihiko.
In: Nishinihon Journal of Urology, Vol. 67, No. 4, 04.2005, p. 168-175.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Regulation of dendritic cell activation and autoimmunity by SOCS1
AU - Hanada, Toshikatsu
AU - Yoshimura, Akihiko
PY - 2005/4
Y1 - 2005/4
N2 - 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.
AB - 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.
KW - Autoimmune diseases
KW - Cytokine
KW - Dendritic cell
KW - Inflammation
KW - Signal transduction
KW - Tumorigenesiss
UR - http://www.scopus.com/inward/record.url?scp=18244408534&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=18244408534&partnerID=8YFLogxK
M3 - Article
VL - 67
SP - 168
EP - 175
JO - Nishinihon Journal of Urology
JF - Nishinihon Journal of Urology
SN - 0029-0726
IS - 4
ER -