| First Author | O'Connor T | Year | 2019 |
| Journal | Cancer Cell | Volume | 36 |
| Issue | 3 | Pages | 250-267.e9 |
| PubMed ID | 31526758 | Mgi Jnum | J:279350 |
| Mgi Id | MGI:6360754 | Doi | 10.1016/j.ccell.2019.08.001 |
| Citation | O'Connor T, et al. (2019) Age-Related Gliosis Promotes Central Nervous System Lymphoma through CCL19-Mediated Tumor Cell Retention. Cancer Cell 36(3):250-267.e9 |
| abstractText | How lymphoma cells (LCs) invade the brain during the development of central nervous system lymphoma (CNSL) is unclear. We found that NF-kappaB-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. |
