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Athymic mice reveal a requirement for T-cell-microglia interactions in establishing a microenvironment supportive of Nf1 low-grade glioma growth.

Pan, Yuan; Xiong, Min; Chen, Ran; Ma, Yu; Corman, Courtney; Maricos, Meron; Kindler, Urs; Semtner, Marcus; Chen, Yi-Hsien; Dahiya, Sonika; Gutmann, David H.
Genes Dev; 32(7-8): 491-496, 2018 04 01.
Artigo em Inglês | MEDLINE | ID: mdl-29632086
Pediatric low-grade gliomas (LGGs) frequently do not engraft in immunocompromised mice, limiting their use as an experimental platform. In contrast, murine Neurofibromatosis-1 (Nf1) optic LGG stem cells (o-GSCs) form glioma-like lesions in wild-type, but not athymic, mice following transplantation. Here, we show that the inability of athymic mice to support o-GSC engraftment results from impaired microglia/macrophage function, including reduced expression of Ccr2 and Ccl5, both of which are required for o-GSC engraftment and Nf1 optic glioma growth. Impaired Ccr2 and Ccl5 expression in athymic microglia/macrophages was restored by T-cell exposure, establishing T-cell-microglia/macrophage interactions as critical stromal determinants that support NF1 LGG growth.
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