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Sequestration of T cells in bone marrow in the setting of glioblastoma and other intracranial tumorsChongsathidkiet, Pakawat; Jackson, Christina; Koyama, Shohei; Loebel, Franziska; Cui, Xiuyu; Farber, S Harrison; Woroniecka, Karolina; Elsamadicy, Aladine A; Dechant, Cosette A; Kemeny, Hanna R; Sanchez-Perez, Luis; Cheema, Tooba A; Souders, Nicholas C; Herndon, James E; Coumans, Jean-Valery; Everitt, Jeffrey I; Nahed, Brian V; Sampson, John H; Gunn, Michael D; Martuza, Robert L; Dranoff, Glenn; Curry, William T; Fecci, Peter E
Nature medicine, 09/2018, Letnik: 24, Številka: 9Journal Article
T cell dysfunction contributes to tumor immune escape in patients with cancer and is particularly severe amidst glioblastoma (GBM). Among other defects, T cell lymphopenia is characteristic, yet often attributed to treatment. We reveal that even treatment-naïve subjects and mice with GBM can harbor AIDS-level CD4 counts, as well as contracted, T cell-deficient lymphoid organs. Missing naïve T cells are instead found sequestered in large numbers in the bone marrow. This phenomenon characterizes not only GBM but a variety of other cancers, although only when tumors are introduced into the intracranial compartment. T cell sequestration is accompanied by tumor-imposed loss of S1P1 from the T cell surface and is reversible upon precluding S1P1 internalization. In murine models of GBM, hindering S1P1 internalization and reversing sequestration licenses T cell-activating therapies that were previously ineffective. Sequestration of T cells in bone marrow is therefore a tumor-adaptive mode of T cell dysfunction, whose reversal may constitute a promising immunotherapeutic adjunct.
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