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O'Connor, T. ; Zhou, X.* ; Kosla, J. ; Adili, A. ; Garcia Beccaria, M.* ; Kotsiliti, E. ; Pfister, D. ; Johlke, A.-L. ; Sinha, A.* ; Sankowski, R.* ; Schick, M.* ; Lewis, R.* ; Dokalis, N.* ; Seubert, B. ; Höchst, B.* ; Inverso, D.* ; Heide, D.* ; Zhang, W.* ; Weihrich, P.* ; Manske, K.* ; Wohlleber, D.* ; Anton, M.* ; Hoellein, A.* ; Seleznik, G.M.* ; Bremer, J.* ; Bleul, S.* ; Augustin, H.G.* ; Scherer, F.* ; Koedel, U.* ; Weber, A.* ; Protzer, U. ; Förster, R.* ; Wirth, T.* ; Aguzzi, A.* ; Meissner, F.* ; Prinz, M.* ; Baumann, B.* ; Höpken, U.E.* ; Knolle, P.A.* ; von Baumgarten, L.* ; Keller, U.* ; Heikenwälder, M.

Age-related gliosis promotes central nervous system lymphoma through CCL19-mediated tumor cell retention.

Cancer Cell 36, 250-267.e9 (2019)
Verlagsversion Preprint DOI
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Ccl19 ; Cnsl ; Cxcl12 ; Dlbcl ; Gliosis ; Lymphoma ; Metastasis ; Neuroinflammation ; Pcnsl ; Scnsl
ISSN (print) / ISBN 1535-6108
e-ISSN 1878-3686
Zeitschrift Cancer Cell
Quellenangaben Band: 36, Heft: 3, Seiten: 250-267.e9 Artikelnummer: , Supplement: ,
Verlag Cell Press
Verlagsort Cambridge, Mass.
Begutachtungsstatus Peer reviewed