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CD56bright NK cells are enriched at inflammatory sites and can engage with monocytes in a reciprocal program of

Nicola Dalbeth1, Roger Gundle, Robert J O Davies

  • 1Division of Medicine, Imperial College London, Commonwealth Building, Hammersmith Campus, Du Cane Road, London W12 0NN, UK.

Journal of Immunology (Baltimore, Md. : 1950)
|November 6, 2004
PubMed

Insights

CD56(bright) natural killer (NK) cells accumulate in inflammatory lesions and interact with CD14(+) monocytes. This reciprocal activation amplifies inflammation, potentially driving chronic inflammatory diseases like rheumatoid arthritis.

Area of Science:

  • Immunology
  • Cell Biology
  • Pathogenesis of Inflammatory Diseases

Background:

  • Human natural killer (NK) cells comprise CD56(dim) and CD56(bright) subsets with distinct tissue distributions.
  • CD56(dim) NK cells are predominant in peripheral blood, while CD56(bright) NK cells are more abundant in lymph nodes.

Purpose of the Study:

  • To investigate the role and behavior of CD56(bright) NK cells in inflammatory lesions.
  • To elucidate the interaction between CD56(bright) NK cells and CD14(+) monocytes in the context of inflammation.

Main Methods:

  • Analysis of NK cell subsets in inflammatory lesions across various diseases and anatomical sites.
  • In vitro co-culture experiments to assess cell-cell contact-dependent cytokine production (TNF-alpha and IFN-gamma) between NK cells and monocytes.
  • Monokine (IL-12, IL-15, IL-18) stimulation assays.

Main Results:

  • CD56(bright) NK cells were found to accumulate in inflammatory lesions of diverse clinical conditions.
  • Activated CD56(bright) NK cells promoted TNF-alpha production by CD14(+) monocytes via cell-cell contact.
  • CD14(+) monocytes, in synergy with monokines, promoted IFN-gamma production by CD56(bright) NK cells through cell-cell contact.

Conclusions:

  • CD56(bright) NK cells accumulate in inflammatory sites and engage in reciprocal activation with CD14(+) monocytes.
  • This cell-cell contact-dependent interaction amplifies the inflammatory response.
  • The identified positive feedback loop is implicated in the pathogenesis of chronic inflammatory conditions, including rheumatoid arthritis.

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