Effect of influenza A infection on umbilical cord blood natural killer function regulation with interleukin-15

Syh-Jae Lin1, Po-Jen Cheng, Tzou-Yien Lin

  • 1Division of Asthma, Allergy, and Rheumatology, Chang Gung Memorial Hospital, Taoyuan, Taiwan.

Insights

Infant natural killer (NK) cells show reduced responses to influenza A compared to adults. Interleukin-15 (IL-15) may boost NK cell antiviral activity and interferon-gamma production.

Area of Science:

  • Immunology
  • Virology
  • Infectious Diseases

Background:

  • Influenza A poses a pandemic threat, with infants exhibiting increased susceptibility to severe infections.
  • Natural killer (NK) cells are crucial for innate immunity against viral infections like influenza A.
  • Infant NK cell function may be impaired, contributing to their vulnerability to severe influenza.

Purpose of the Study:

  • To compare natural killer (NK) cell responses to influenza A between newborns and adults.
  • To investigate the role of interleukin-15 (IL-15) in modulating NK cell activity against influenza.

Main Methods:

  • Comparison of NK cell responses using umbilical cord blood (UCB) and adult peripheral blood (APB) mononuclear cells.
  • Analysis of NK cell apoptosis, surface marker expression (NKp46, CD69, CD107a), perforin expression, and cytotoxicity.
  • Assessment of cytokine production (interferon-gamma, tumor necrosis factor-alpha) by NK cells.

Main Results:

  • Influenza A induced dose-dependent NK cell apoptosis and NKp46 down-regulation, more significantly in UCB.
  • Both UCB and APB NK cells upregulated CD69 and CD107a upon influenza exposure, enhanced by IL-15.
  • IL-15 partially restored UCB NK cell perforin expression and K562 cytotoxicity and boosted interferon-gamma and tumor necrosis factor-alpha production.

Conclusions:

  • Neonatal and adult NK cells exhibit distinct responses to influenza A.
  • IL-15 demonstrates potential therapeutic benefits by enhancing NK cell cytotoxic function and interferon-gamma production against influenza.
Abstract