| First Author | Tsukada J | Year | 2005 |
| Journal | Int Immunol | Volume | 17 |
| Issue | 9 | Pages | 1167-78 |
| PubMed ID | 16091384 | Mgi Jnum | J:100705 |
| Mgi Id | MGI:3589324 | Doi | 10.1093/intimm/dxh294 |
| Citation | Tsukada J, et al. (2005) The role of suppressor of cytokine signaling 1 as a negative regulator for aberrant expansion of CD8{alpha}+ dendritic cell subset. Int Immunol 17(9):1167-78 |
| abstractText | The suppressor of cytokine signaling (SOCS) 1 is a negative regulator in multiple cytokine-related aspects to maintain immunological homeostasis. Here, we studied a role of SOCS1 on dendritic cell (DC) maturation in the mice lacking either TCRalpha chain or CD28 in SOCS1-deficient background, and found that the SOCS1 could restore acute phase of inflammatory response in SOCS1-deficient mice. The CD11c(+) CD8(-) DC population in freshly isolated splenic DCs from normal mice highly expressed SOCS1. However, in SOCS1-deficient environment, the proportion of CD8alpha(+) DCs (CD8 DCs) noticeably increased without affecting the cell number of conventional and plasmacytoid DC populations. This population revealed the CD11c(dull) CD8alpha(+) CD11b(-) CD45RA(-) B220(-) phenotype, which is a minor population in normal mice. Localization of the abnormal CD8 DCs in splenic microenvironments was mainly restricted to deep within red pulp. The CD8 DCs secrete a large amount of IFN-gamma, IL-12 and B lymphocyte stimulator/B cell activation factor of the tumor necrosis factor family in response to LPS and CpG stimulation. This is responsible for the development of DC-mediated systemic autoimmunity in the old age of SOCS1-deficient mice. Moreover, the CD8 DC subsets expressed more indoleamine 2,3-dioxygenase and IL-10, and hence inhibit the allogeneic proliferative T cell response and antigen-induced T(h)1 responses. Therefore, SOCS1 expression during DC maturation plays a role in surveillance in controlling the aberrant expansion of abnormal DC subset to maintain homeostasis of immune system. |
