Tumor microenvironment (TME)-driven immune suppression in B cell malignancy

Nicole S. Nicholas, Benedetta Apollonio, Alan G. Ramsay*

*Corresponding author for this work

    Research output: Contribution to journalArticlepeer-review

    92 Citations (Scopus)

    Abstract

    Immune checkpoint blockade antibodies and immunomodulatory drugs can unleash anti-tumor T cell immunity and mediate durable cancer regressions. However, only a fraction of patients currently respond to immunotherapy. Lymphoid malignancies are known to have clinically exploitable immune sensitivity and their intrinsic lymphoid tumor-microenvironment (TME) should make them natural targets for immunotherapy. However, accumulating evidence is showing that malignant cells engage in novel associations/interdependencies with reprogrammed immune and stromal cells in the TME that provide crucial contributions to the licencing of tumour progression and immune evasion (suppression of antitumor immune responses). In this review, we outline TME-driven contributions to the licencing of immune evasion mechanisms including the expression and activity of the immune checkpoint network, focussing on two types of B cell malignancy: indolent chronic lymphocytic leukemia (CLL) and aggressive diffuse large B-cell lymphoma (DLBCL). We also highlight recent therapeutic strategies to re-educate the TME to have anti-tumorigenic effects. This article is part of a Special Issue entitled: Tumor Microenvironment Regulation of Cancer Cell Survival, Metastasis, Inflammation, and Immune Surveillance edited by Peter Ruvolo and Gregg L. Semenza.

    Original languageEnglish
    Pages (from-to)471-482
    Number of pages12
    JournalBiochimica et biophysica acta-Molecular cell research
    Volume1863
    Issue number3
    Early online date7 Nov 2015
    DOIs
    Publication statusPublished - 1 Mar 2016

    Keywords

    • CLL
    • CTLA-4
    • DLBCL
    • Immune checkpoint blockade
    • Immune evasion
    • Lenalidomide
    • PD-1
    • PD-L1
    • T cells

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