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Related Concept Videos

Tumor Immunotherapy01:27

Tumor Immunotherapy

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Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
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HDAC6 Inhibition Alleviates CLL-Induced T-Cell Dysfunction and Enhances Immune Checkpoint Blockade Efficacy in the

Kamira Maharaj1,2, John J Powers1, Melanie Mediavilla-Varela1

  • 1Department of Immunology, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL, United States.

Frontiers in Immunology
|December 17, 2020
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Summary

HDAC6 inhibition improves immune function in chronic lymphocytic leukemia (CLL) by reducing immunosuppressive factors on CLL B cells and enhancing T-cell responses. This suggests HDAC6 inhibitors combined with immunotherapy could be a promising treatment strategy for CLL.

Keywords:
B cellHDAC6PD-1PD-L1T cellchronic lymphocytic leukemiahistone deacetylaseimmune checkpoint

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Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Chronic lymphocytic leukemia (CLL) is characterized by immune dysfunction, leading to increased susceptibility to infections.
  • CLL pathogenesis involves T-cell exhaustion, immune checkpoint upregulation, and regulatory T cells, creating an immunosuppressive tumor microenvironment.
  • Histone deacetylase 6 (HDAC6) plays a role in regulating immune cell phenotype and function.

Purpose of the Study:

  • To investigate the immunomodulatory effects of HDAC6 inhibition on CLL B cells and T cells.
  • To explore the potential of HDAC6 inhibition in combination with immune checkpoint blockade for CLL treatment.

Main Methods:

  • Utilized the Eμ-TCL1 adoptive transfer murine model for CLL.
  • Employed genetic silencing and pharmacological inhibition of HDAC6.
  • Assessed changes in CLL B cell surface markers (e.g., PD-L1), cytokine levels (e.g., IL-10), and T-cell phenotype (coinhibitory molecules, activation status).
  • Evaluated the efficacy of combination treatment with an HDAC6 inhibitor (ACY738) and anti-PD-1/anti-PD-L1 antibodies.

Main Results:

  • HDAC6 inhibition reduced PD-L1 expression and IL-10 levels on CLL B cells.
  • HDAC6 inhibition led to an improved T-cell phenotype, characterized by altered coinhibitory molecules and activation status.
  • HDAC6 inhibition's effects on T cells were partly attributed to reduced tumor burden and CLL B cell immunomodulation.
  • HDAC6 inhibition modulated CLL B cell phenotype via hyperacetylation of HSP90 and subsequent JAK/STAT pathway inhibition.
  • Combination therapy of ACY738 with anti-PD-1/anti-PD-L1 antibodies enhanced anti-tumor efficacy and increased cytotoxic CD8+ T cells.

Conclusions:

  • HDAC6 inhibition demonstrates beneficial immunomodulatory effects in CLL, alleviating immunosuppression.
  • HDAC6 inhibition can alter CLL B cell phenotype and T-cell function, potentially by targeting the HSP90/JAK/STAT pathway.
  • Combining HDAC6 inhibitors with immune checkpoint blockade represents a promising therapeutic strategy for CLL, warranting further clinical investigation.