論文 - 詳細
| RRC ID | 87173 |
|---|---|
| 著者 | Fleig S, Kapanadze T, Bernier-Latmani J, Lill JK, Wyss T, Gamrekelashvili J, Kijas D, Liu B, Hüsing AM, Bovay E, Jirmo AC, Halle S, Ricke-Hoch M, Adams RH, Engel DR, von Vietinghoff S, Förster R, Hilfiker-Kleiner D, Haller H, Petrova TV, Limbourg FP. |
| タイトル | Loss of vascular endothelial notch signaling promotes spontaneous formation of tertiary lymphoid structures. |
| ジャーナル | Nat Commun |
| Abstract |
Tertiary lymphoid structures (TLS) are lymph node-like immune cell clusters that emerge during chronic inflammation in non-lymphoid organs like the kidney, but their origin remains not well understood. Here we show, using conditional deletion strategies of the canonical Notch signaling mediator Rbpj, that loss of endothelial Notch signaling in adult mice induces the spontaneous formation of bona fide TLS in the kidney, liver and lung, based on molecular, cellular and structural criteria. These TLS form in a stereotypical manner around parenchymal arteries, while secondary lymphoid structures remained largely unchanged. This effect is mediated by endothelium of blood vessels, but not lymphatics, since a lymphatic endothelial-specific targeting strategy did not result in TLS formation, and involves loss of arterial specification and concomitant acquisition of a high endothelial cell phenotype, as shown by transcriptional analysis of kidney endothelial cells. This indicates a so far unrecognized role for vascular endothelial cells and Notch signaling in TLS initiation. |
| 巻・号 | 13(1) |
| ページ | 2022 |
| 公開日 | 2022-4-19 |
| DOI | 10.1038/s41467-022-29701-x |
| PII | 10.1038/s41467-022-29701-x |
| PMID | 35440634 |
| PMC | PMC9018798 |
| MeSH | Animals Endothelial Cells Endothelium, Vascular Inflammation Mice Receptors, Notch / genetics Signal Transduction Tertiary Lymphoid Structures* |
| IF | 12.121 |
| オルトメトリクス指標 |
オルトメトリクス指標項目
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| 最多言及媒体 | X(Twitter) |
| 各媒体での言及数の合計 | 82 |
| 過去6か月間でのオルトメトリクス指標の変動値 | 0.0 |
| リソース情報 | |
| 実験動物マウス | RBRC01071 |