Journal Article

DKFZ-2019-02268

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Age-Related Gliosis Promotes Central Nervous System Lymphoma through CCL19-Mediated Tumor Cell Retention.

O'Connor, T. (First author)DKFZ* ; Zhou, X. ; Kosla, J.DKFZ* ; Adili, A. ; Garcia Beccaria, M.DKFZ* ; Kotsiliti, E.DKFZ* ; Pfister, D.DKFZ* ; Johlke, A.-L. ; Sinha, A. ; Sankowski, R. ; Schick, M. ; Lewis, R. ; Dokalis, N. ; Seubert, B. ; Höchst, B. ; Inverso, D.DKFZ* ; Heide, D.DKFZ* ; Zhang, W. ; Weihrich, P. ; Manske, K. ; Wohlleber, D. ; Anton, M. ; Hoellein, A. ; Seleznik, G. ; Bremer, J. ; Bleul, S. ; Augustin, H. G.DKFZ* ; 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. (Last author)DKFZ*

2019
Elsevier New York, NY

This record in other databases:  

Please use a persistent id in citations: doi:10.1016/j.ccell.2019.08.001

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.

Note: DKFZ-ZMBH Alliance

---

Contributing Institute(s):

1. Chronische Entzündung und Krebs (F180)
2. Vaskuläre Onkologie und Metastasierung (A190)
3. DKTK Heidelberg (L101)

Research Program(s):

1. 316 - Infections and cancer (POF3-316) (POF3-316)

Appears in the scientific report 2019

---

Database coverage:
; BIOSIS Previews ; Clarivate Analytics Master Journal List ; Current Contents - Clinical Medicine ; Current Contents - Life Sciences ; Ebsco Academic Search ; IF >= 20 ; JCR ; NCBI Molecular Biology Database ; SCOPUS ; Science Citation Index ; Science Citation Index Expanded ; Web of Science Core Collection

---