Extended Data Fig. 10: Working model. | Nature Immunology

Extended Data Fig. 10: Working model.

From: Kunitz-type protease inhibitor TFPI2 remodels stemness and immunosuppressive tumor microenvironment in glioblastoma

Extended Data Fig. 10

a, Illustration shows a proposed mechanism for the TFPI2 and its associated signaling axis in regulating self-renewal of glioma stem cells (GSCs) and GSC-microglia symbiosis in GBM. TFPI2 is amplified in GBM and essential for tumor progression. Upon secreting from GSCs, TFPI2 promotes GSC self-renewal by activating the JNK-STAT3 signaling pathway. Secreted TFPI2 binds to CD51 on microglia to promote microglia infiltration and immunosuppressive polarization via activation of STAT6 signaling. Consequently, these activated microglia inhibit the infiltration and activation of T cells and damage their tumor killing potential. b, Inhibition of TFPI2-CD51-STAT6 signaling axis impairs tumor progression by reducing immunosuppressive microglia and activating T cell-mediated antitumor immunity and synergizes with anti-PD1 therapy in GBM. This image was created with BioRender.com.

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