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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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T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
Naive T cells that have not yet encountered an antigen express two primary CD...
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Cytotoxic T Cells-mediated Immune Response01:27

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Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
Immunological surveillance is the ability of immune cells to monitor and eliminate infected cells with intracellular pathogens, neoplastically transformed cells, and cells with non-self antigens. Cytotoxic T cells and NK...
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CD137 Costimulation Counteracts TGFβ Inhibition of NK-cell Antitumor Function.

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Urelumab, an anti-CD137 agonist, enhances natural killer (NK) cell immunotherapy by overcoming TGFβ-induced suppression. This approach boosts NK cell proliferation, effector functions, and tumor-homing capabilities, improving cancer treatment potential.

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Area of Science:

  • Immunology
  • Cancer Biology
  • Immunotherapy

Background:

  • Natural killer (NK) cells are crucial for cancer immunotherapy.
  • TGFβ signaling can suppress NK cell activity, limiting their effectiveness.
  • Overcoming this immunosuppression is key to enhancing NK cell-based therapies.

Purpose of the Study:

  • To investigate if the anti-CD137 agonist urelumab can overcome TGFβ-mediated inhibition of human NK cells.
  • To analyze the effects of CD137 costimulation on NK cell proliferation, function, and tumor-homing properties.
  • To explore the translational relevance of targeting the CD137 axis in HER2-positive breast cancer.

Main Methods:

  • Transcriptomic, immunophenotypic, and functional analyses of human NK cells.
  • Culture of NK cells with TGFβ1 and CD137 agonist (urelumab).
  • Assessment of cytotoxicity in breast carcinoma-derived multicellular cultures treated with trastuzumab and urelumab.
  • Bioinformatic analysis of clinical data from HER2-positive breast cancer patients.

Main Results:

  • Urelumab rescued NK cell proliferation inhibited by TGFβ and enhanced expression of activating receptors and effector molecules.
  • CD137 costimulation promoted tumor-homing features (CXCR3, CD103) and enhanced NK cell cytotoxicity.
  • Urelumab treatment in combination with trastuzumab increased NK cell infiltration and cytokine production in breast cancer models.
  • IFNG was identified as a key driver linking NK cells to clinical response in trastuzumab-treated patients.

Conclusions:

  • CD137 costimulation is a viable strategy to overcome TGFβ-induced suppression of NK cell antitumor responses.
  • Targeting the CD137 axis holds translational potential for enhancing NK cell-based cancer immunotherapies, particularly in HER2-positive breast cancer.
  • Urelumab represents a promising therapeutic target for boosting NK cell function in cancer treatment.