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Updated: Aug 25, 2025

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NSAIDs affect dendritic cell cytokine production.

Tonke K Raaijmakers1,2, Renske J E van den Bijgaart1, Gert Jan Scheffer2

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Non-steroid anti-inflammatory drugs (NSAIDs) can impair dendritic cell (DC) function, potentially affecting cancer immunotherapy. This study investigated NSAID impacts on DC cross-presentation, co-stimulation, and cytokine production for anti-tumor immunity.

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Area of Science:

  • Immunology
  • Cancer Research
  • Pharmacology

Background:

  • Immunotherapy is a cornerstone of cancer treatment, with dendritic cells (DCs) crucial for initiating anti-tumor immune responses.
  • DCs present tumor antigens to CD8+ T cells, a key step in adaptive immunity.
  • The impact of commonly used non-steroid anti-inflammatory drugs (NSAIDs) on DC function remains largely unexplored.

Purpose of the Study:

  • To investigate the effects of NSAIDs (diclofenac, ibuprofen, celecoxib) on critical DC functions.
  • To assess NSAID influence on antigen cross-presentation, co-stimulatory molecule expression, and cytokine production.
  • To understand how NSAIDs might impact T cell priming and the efficacy of cancer immunotherapy.

Main Methods:

  • Human monocyte-derived and murine bone-marrow derived DCs were utilized.
  • DCs were exposed to diclofenac, ibuprofen, and celecoxib.
  • Key DC functions including antigen cross-presentation, co-stimulatory marker expression, and cytokine production were analyzed.

Main Results:

  • NSAID exposure diminished Toll-like receptor (TLR)-induced pro-inflammatory cytokine excretion by DCs.
  • NSAID exposure also reduced anti-inflammatory cytokine excretion by DCs.
  • These effects were observed in both human and murine DC models.

Conclusions:

  • Various NSAIDs can significantly affect dendritic cell function.
  • NSAID-induced alterations in DC function may compromise their ability to prime T cells.
  • Further research is warranted to determine the clinical implications of NSAID use on cancer immunotherapy effectiveness.