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Reciprocal human dendritic cell-natural killer cell interactions induce antitumor activity following tumor cell

Robin J Prestwich1, Fiona Errington, Lynette P Steele

  • 1Leeds Institute of Molecular Medicine, University of Leeds, Leeds, United Kingdom;

Journal of Immunology (Baltimore, Md. : 1950)
|September 8, 2009
PubMed

Insights

Reovirus therapy activates dendritic cells (DCs) to recruit and activate natural killer (NK) cells, enhancing antitumor immunity. This study reveals how reovirus-infected tumor cells stimulate DCs, leading to robust NK cell-mediated tumor cell killing.

Area of Science:

  • Immunology
  • Virology
  • Cancer Therapy

Background:

  • Oncolytic virotherapy uses viruses to fight cancer, but its impact on the innate immune system is not fully understood.
  • Reovirus therapy's ability to generate adaptive antitumor immunity is known, yet its innate immune interactions require further investigation.

Purpose of the Study:

  • To investigate the innate immunological effects of reovirus therapy using a human in vitro system.
  • To explore the potential of reovirus therapy to activate natural killer (NK) cell-mediated antitumor activity.

Main Methods:

  • Utilized a human in vitro system involving dendritic cells (DCs) loaded with reovirus-infected melanoma cells (DC-MelReo).
  • Co-cultured DC-MelReo with peripheral blood mononuclear cells (PBMCs) and purified NK cells to assess immune responses.
  • Measured cytokine production, chemokine secretion, cell-to-cell contact-dependent interactions, and NK cell activation markers (CD69).

Main Results:

  • DC-MelReo induced IFN-gamma production in NK cells and secreted chemokines (CCL2, 3, 4, 5, 7, 8, 11, CXCL10) that promoted NK cell chemotaxis.
  • Reciprocal DC maturation and NK cell activation (CD69 up-regulation) occurred upon co-culture, dependent on cell contact and IL-12.
  • DC-MelReo treatment led to type I IFN-dependent NK cell cytotoxicity against tumor cells.

Conclusions:

  • Reovirus infection of tumor cells can activate DCs, which in turn recruit, activate, and enhance NK cell cytotoxicity.
  • Reciprocal interactions between DCs and NK cells following reovirus therapy may significantly alter the tumor microenvironment.
  • These DC-NK cell interactions are crucial for mediating tumor regression in oncolytic virotherapy.

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