Reverse interferon signature is characteristic of antigen-presenting cells in human and rat spondyloarthritis.
Reverse interferon signature is characteristic of antigen-presenting cells in human and rat spondyloarthritis.
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DOI：
10.1002/art.38318
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发表时间：
2014-04
影响因子：
13.3
通讯作者：
Breban, Maxime
中科院分区：
文献类型：
--
作者：
Fert, Ingrid;Cagnard, Nicolas;Glatigny, Simon;Letourneur, Franck;Jacques, Sebastien;Smith, Judith A.;Colbert, Robert A.;Taurog, Joel D.;Chiocchia, Gilles;Araujo, Luiza M.;Breban, Maxime
In rats transgenic for HLA-B27 (B27 rat), the development of a disorder mimicking spondyloarthritis (SpA) is tightly correlated with DCs dysfunction. To dissect the underlying mechanisms, we studied the transcriptome of ex vivo purified CD103+CD4+ DCs. Transcriptome analysis was performed on splenic CD103+CD4+ DCs from B27 and control rats. Transcriptional changes for selected genes were confirmed by quantitative reverse transcriptase–polymerase chain reaction. A meta-analysis was further performed, between the rat data and published gene expression analysis performed on macrophages from ankylosing spondylitis (AS) patients. IFN signaling was the most significantly affected pathway in B27 rat DCs, with a majority of genes connected to IFN being under-expressed, as compared to controls. This pattern was already present at disease onset, persisted over time, and was conserved in two disease-prone B27 rat lines. In B27 rat DCs, we further found an upregulation of suppressor of cytokine signaling-3 that may account for reverse IFN signaling, and a down-regulation of IL-27, a cytokine that opposes Th17 differentiation and promotes regulatory T cells. The meta-analysis between rat conventional DCs and human monocyte-derived macrophages data revealed 7 IFN-regulated genes that were negatively regulated both in human and rat SpA: IRF1, STAT1, CXCL9, CXCL10, IFIT3, DDX60 and EPSTI1. Our results suggest that expression of HLA-B27 leads to a defect in IFN-γ signaling in antigen-presenting cells, shared between B27 rats and SpA patients, which may result in Th17 expansion and regulatory T cell alteration, as shown in B27 rats, and contribute to disease pathogenesis.
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大鼠脾树突状细胞表达天然杀伤细胞受体蛋白1（NKR-P1），具有细胞毒性活性，可以通过CA2+依赖性机制选择靶标。
DOI：
10.1084/jem.186.3.467
发表时间：
1997-08-04
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Josien R;Heslan M;Soulillou JP;Cuturi MC
通讯作者：
Cuturi MC
影响因子：
--
作者：
Fert, Ingrid;Glatigny, Simon;Breban, Maxime
通讯作者：
Breban, Maxime
影响因子：
8.7
作者：
Colbert RA;DeLay ML;Klenk EI;Layh-Schmitt G
通讯作者：
Layh-Schmitt G
影响因子：
32.4
作者：
Huber S;Gagliani N;Esplugues E;O'Connor W Jr;Huber FJ;Chaudhry A;Kamanaka M;Kobayashi Y;Booth CJ;Rudensky AY;Roncarolo MG;Battaglia M;Flavell RA
通讯作者：
Flavell RA
影响因子：
5.5
作者：
Choi, S. T.;Kim, J. H.;Lee, S. -K.
通讯作者：
Lee, S. -K.