期刊
CANCER CELL
卷 36, 期 3, 页码 250-+出版社
CELL PRESS
DOI: 10.1016/j.ccell.2019.08.001
关键词
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资金
- DFG [5892/5-1, SFB824]
- Helmholtz Preclinical Comprehensive Cancer Center (PCCC)
- ERC Starting (LiverCancerMechanisms) grant
- ERC Consolidator (HepatoMetaboPath) grant
- Stiftung fur biomedizinische Forschung
- U.K., Deutsche Krebshilfe [111305, 111944]
- Helmholtz-Gemeinschaft, Zukunftsthema Immunology and Inflammation [ZT-0027]
- Else Kroner-Fresenius-Stiftung [2014_A265]
- Bayerische Gleichstellungsforderung der LMU
- Forderprogramm fur Forschung und Lehre der LMU [863]
- Berta-Ottenstein-Programme
- BMBF [031B0686B]
- ALTF [539-2018]
- [SFBTR179]
- [SFBTR209]
- [SFBTR1335]
- [SFB 1335]
How lymphoma cells (LCs) invade the brain during the development of central nervous system lymphoma (CNSL) is unclear. We found that NF-KB-induced gliosis promotes CNSL in immunocompetent mice. Gliosis elevated cell-adhesion molecules, which increased LCs in the brain but was insufficient to induce CNSL. Astrocyte-derived CCL19 was required for gliosis-induced CNSL. Deleting CCL19 in mice or CCR7 from LCs abrogated CNSL development. Two-photon microscopy revealed LCs transiently entering normal brain parenchyma. Astrocytic CCL19 enhanced parenchymal CNS retention of LCs, thereby promoting CNSL formation. Aged, gliotic wild-type mice were more susceptible to forming CNSL than young wild-type mice, and astrocytic CCL19 was observed in both human gliosis and CNSL. Therefore, CCL19-CCR7 interactions may underlie an increased age-related risk for CNSL.
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