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Immunobiology

Session: Poster Session

IMMU-31 - B-cell therapy (BVax) promotes CD8 T cells' persistence and function in the glioblastoma microenvironment by maintaining their stem-like features.

Friday, November 17, 2023
7:30 PM – 9:30 PM PT
Location: Exhibit Hall A/B
Non-CME

    Author(s)

  • HW

    Hanxiao Wan

    Northwestern University
    Chicago, United States

    • Author(s)

  • David Hou

    Northwestern University
    Chicago, Illinois, United States

    • Poster Presenter(s)

  • Joshua L. Katz

    Northwestern University
    Chicago, United States

    • Author(s)

  • SW

    Si Wang

    Northwestern University
    Chicago, Illinois, United States

  • Brandyn Castro

    Northwestern University
    Chicago, Illinois, United States

  • Tzu-Yi Chia

    Northwestern University
    Chicago, United States

  • Gustavo Ignacio Vazquez Cervantes

    Northwestern University
    Chicago, Illinois, United States

  • Leah Billingham

    Northwestern University
    Chicago, United States

  • Victor A. Arrieta

    Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University
    Chicago, Illinois, United States

  • YH

    Yu Han

    Northwestern University
    Chicago, Illinois, United States

  • AL

    Aurora Lopez-Rosas

    Northwestern University
    Chicago, Illinois, United States

  • PZ

    Peng Zhang

    Northwestern University
    Chicago, United States

  • Jason Miska

    Northwestern University
    Chicago, United States

  • CL

    Catalina L. Lee-Chang

    Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University
    Chicago, Illinois, United States

The last decade witnessed tremendous improvement in immunotherapy to treat cancers. Its application in GBM has been particularly challenging due to the immunosuppressive tumor microenvironment, which greatly challenges T-cell infiltration and function. We developed a B-cell therapy with potent antigen-presenting functions that promote CD8+ tumor tropism and persistence in the tumor microenvironment. The present study investigates how BVax activates CD8+ T cells differently from other professional APCs like dendritic cells (DC) that could explain the persistence of CD8+ T cells in the tumor microenvironment. Upon in vitro activation by coculturing with BVax, most CD8+ T cells proliferated into TCF+ PD1- intermediate state, with CD44+ CD62L+ memory phenotype. Less than 10% of CD8+ were in the terminally-proliferation state. In contrast, DCs preferentially expanded TCF- PD1+ terminally-proliferating CD8+ T cells that were exhibiting CD44+ CD62L- effector phenotype. In vivo, activation of CD8+ T cells by co-injecting BVax or DC with CD8+ T cells to CT2A-bearing mice indicated that BVax promoted the proliferation of tumor-reactive CD8 T cells while maintaining the low PD1+ expression. Re-exposing the ex vivo-activated CD8+ T cells to tumor by adoptive transferring them to CT2A tumor-bearing mice revealed that BVax elicited immunological memory and potentiated GzmB+ production of CD8+ T cells. This study suggests that BVax and DC have distinctive interactions with CD8+ T cells, with the former poise CD8+ T cells at a more stem-like state, allowing them to differentiate upon tumor encounter.