| Literature DB >> 31526758 |
Tracy O'Connor1, Xiaolan Zhou2, Jan Kosla3, Arlind Adili4, Maria Garcia Beccaria5, Elena Kotsiliti3, Dominik Pfister3, Anna-Lena Johlke4, Ankit Sinha6, Roman Sankowski7, Markus Schick8, Richard Lewis8, Nikolaos Dokalis7, Bastian Seubert4, Bastian Höchst9, Donato Inverso10, Danijela Heide5, Wenlong Zhang11, Petra Weihrich12, Katrin Manske9, Dirk Wohlleber9, Martina Anton9, Alexander Hoellein8, Gitta Seleznik13, Juliane Bremer13, Sabine Bleul14, Hellmut G Augustin15, Florian Scherer14, Uwe Koedel11, Achim Weber16, Ulrike Protzer4, Reinhold Förster17, Thomas Wirth12, Adriano Aguzzi13, Felix Meissner6, Marco Prinz18, Bernd Baumann12, Uta E Höpken19, Percy A Knolle9, Louisa von Baumgarten11, Ulrich Keller20, Mathias Heikenwalder21.
Abstract
How lymphoma cells (LCs) invade the brain during the development of central nervous system lymphoma (CNSL) is unclear. We found that NF-κB-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.Entities:
Keywords: CCL19; CNSL; CXCL12; DLBCL; PCNSL; SCNSL; gliosis; lymphoma; metastasis; neuroinflammation
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Year: 2019 PMID： 31526758 DOI： 10.1016/j.ccell.2019.08.001
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743