| First Author | Hanada T | Year | 2003 |
| Journal | Immunity | Volume | 19 |
| Issue | 3 | Pages | 437-50 |
| PubMed ID | 14499118 | Mgi Jnum | J:85811 |
| Mgi Id | MGI:2677084 | Doi | 10.1016/s1074-7613(03)00240-1 |
| Citation | Hanada T, et al. (2003) Suppressor of cytokine signaling-1 is essential for suppressing dendritic cell activation and systemic autoimmunity. Immunity 19(3):437-50 |
| abstractText | 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-gamma and interleukin-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 on a SOCS1(-/-) background. In these mice, DCs were accumulated in the thymus and spleen and produced high levels of BAFF/BLyS and APRIL, resulting in the aberrant expansion of B cells and autoreactive antibody production. SOCS1-deficient DCs efficiently stimulated B cell proliferation in vitro and autoantibody production in vivo. These results indicate that SOCS1 plays an essential role in the normal DC functions and suppression of systemic autoimmunity. |
