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Medium-Chain Fatty Acid Receptor GPR84 Modulates Cytotoxic CD8 T-cell Antitumor Immunity through Metabolic

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Inhibiting GPR84 enhances CD8+ T cell function, metabolism, and antitumor activity. Blocking this receptor boosts T cell proliferation, cytokine production, and energy, improving adoptive cellular therapies.

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Area of Science:

  • Immunology
  • Cell Metabolism
  • Cancer Therapy

Background:

  • GPR84, a medium-chain free fatty acid receptor, is primarily found in myeloid cells.
  • It is known to enhance pro-inflammatory myeloid cell responses and regulate metabolic homeostasis.
  • The role of GPR84 in T cell function and metabolism is not well understood.

Purpose of the Study:

  • To investigate the impact of GPR84 modulation on CD8+ T cell function and metabolism.
  • To assess the effect of GPR84 on antitumor immunity in adoptive cellular therapy models.

Main Methods:

  • In vitro studies involving pharmacological antagonism (GLPG1205) or genetic deletion of GPR84.
  • In vitro studies involving GPR84 agonism (DL175).
  • Assessment of T cell differentiation, proliferation, cytokine production, cytotoxicity, and metabolic activity (glucose uptake, glycolysis, oxidative phosphorylation, ATP production).
  • In vivo evaluation in adoptive cellular therapy models using antigen-specific CD8+ T cells.

Main Results:

  • GPR84 antagonism or deletion promoted CD8+ T cell differentiation, proliferation, cytokine production, and cytotoxicity.
  • These functional enhancements were associated with increased metabolic activity, including glucose uptake, glycolysis, oxidative phosphorylation, and ATP production.
  • GPR84 agonism led to reduced T cell function and a quiescent metabolic profile.
  • In adoptive cellular therapy models, GPR84 antagonism or deletion significantly enhanced antitumor effects.

Conclusions:

  • GPR84 inhibition improves CD8+ T cell function and metabolic fitness.
  • Blocking GPR84 holds potential for enhancing the efficacy of adoptive cellular therapies.
  • Targeting GPR84 represents a promising strategy for cancer immunotherapy.