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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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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
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Updated: Jun 5, 2025

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Tumor-Expressed SPPL3 Supports Innate Antitumor Immune Responses.

Tamara Verkerk1,2, Antonius A de Waard1,2, Sofie J I Koomen1,2

  • 1Department of Immunopathology, Sanquin Research, Amsterdam, The Netherlands.

European Journal of Immunology
|December 10, 2024
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Summary
This summary is machine-generated.

Tumor cells lacking signal peptide peptidase like 3 (SPPL3) evade immune cells by altering glycosphingolipid (GSL) expression. This study shows SPPL3 deficiency impairs innate immune cell recognition and killing of tumor cells.

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Area of Science:

  • Immunology
  • Cancer Biology
  • Glycobiology

Background:

  • Effective antitumor responses depend on immune cells recognizing tumor cells via specific receptors.
  • Tumors can evade immune detection by manipulating receptor-ligand interactions.
  • Neolacto-series glycosphingolipids (nsGSLs) are implicated in tumor immune escape, with their production regulated by β1,3-N-acetylglucosaminyltransferase 5 (B3GNT5).

Purpose of the Study:

  • To investigate the impact of signal peptide peptidase like 3 (SPPL3) deficiency and elevated nsGSLs in tumor cells on innate immune recognition.
  • To determine the antitumor efficacy of neutrophils, natural killer (NK) cells, and γδ T cells against SPPL3-deficient tumor cells.

Main Methods:

  • Assessing the susceptibility of SPPL3-deficient tumor cells to trogocytosis by neutrophils and killing by NK cells and γδ T cells.
  • Investigating the mechanistic role of SPPL3 and nsGSL expression in immune cell interactions.
  • Analyzing the influence of receptor proximity and ligand affinity on SPPL3-mediated immune evasion using antibodies.

Main Results:

  • SPPL3-deficient tumor cells exhibited reduced susceptibility to trogocytosis by neutrophils and killing by γδ T cells, mediated by nsGSL modulation.
  • SPPL3 deficiency also reduced NK cell-mediated killing, but this effect was independent of nsGSL levels.
  • SPPL3 expression in tumor cells alters immune cell crosstalk via the receptor-ligand interactome, promoting escape from both adaptive and innate immunity.

Conclusions:

  • SPPL3 plays a critical role in tumor immune escape by modulating glycosphingolipid expression and influencing interactions with innate immune cells.
  • Targeting SPPL3 or GSL synthesis may enhance the efficacy of immunotherapies that rely on immune cell activation.
  • Further research into combining GSL synthesis inhibitors with immune cell-activating therapies is warranted.