期刊
JOURNAL OF IMMUNOLOGY
卷 186, 期 4, 页码 2192-2200出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1000475
关键词
-
类别
资金
- Ministerio de Educacion y Ciencia [BFU2008-01493-BMC]
- Ministerio de Sanidad y Consumo
- Instituto de Salud Carlos III (Spanish Network for the Research in Infectious Diseases) [REIPI RD06/0008]
- Red de Investigacion en SIDA, RIS [RD06/0006/1016]
- Fundacion para la Investigacion y Prevencion del SIDA [FIPSE 36663/07]
- Fundacion Mutua Madrilena
- Ministerio de Educacion y Ciencia and Fundacion Ramon Areces (XIV Concurso Nacional) [SAF2006-08615]
- Instituto de Salud Carlos III [PI08/1208]
- Ministerio de Sanidad y Consumo [CP06/00199]
Dendritic cell-specific ICAM-3-grabbing nonintegrin (DC-SIGN; CD209) is a human pathogen-attachment C-type lectin with no obvious murine ortholog and for which ligation leads to enhanced anti-inflammatory cytokine release and altered proinflammatory cytokine production. Although induced by IL-4 in monocytes and considered as a DC marker, DC-SIGN expression on human APCs under homeostatic conditions is so far unexplained. We report in this study that M-CSF enhances DC-SIGN expression on in vitro derived anti-inflammatory macrophages and that M-CSF mediates the induction of DC-SIGN by fibroblast-and tumor cell-conditioned media. The M-CSF-inducible DC-SIGN expression along monocyte-to-macrophage differentiation is dependent on JNK and STAT3 activation, potentiated by STAT3-activating cytokines (IL-6, IL-10), and abrogated by the M1-polarizing cytokine GM-CSF. In pathological settings, DC-SIGN expression is detected in tumor tissues and on ex vivo-isolated CD14(+) CD163(+) IL-10-producing tumor-associated macrophages. Importantly, DC-SIGN Abs reduced the release of IL-10 from macrophages exposed to Lewis(x)-expressing SKBR3 tumor cells. These results indicate that DC-SIGN is expressed on both wound-healing (IL-4-dependent) and regulatory (M-CSF-dependent) alternative (M2) macrophages and that DC-SIGN expression on tumor-associated macrophages might help tumor progression by contributing to the maintenance of an immunosuppressive environment. The Journal of Immunology, 2011, 186: 2192-2200.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据