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Cutting edge: IL-15-independent NK cell response to mouse cytomegalovirus infection

Joseph C Sun1, Averil Ma, Lewis L Lanier

  • 1Department of Microbiology and Immunology, University of California, San Francisco, CA 94143-0414, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|August 4, 2009
PubMed

Insights

Natural killer (NK) cells surprisingly expand during viral infections independently of IL-15. This study reveals NK cells can proliferate and function without common gamma signaling cytokines, challenging existing models of immune response.

Area of Science:

  • Immunology
  • Virology
  • Cellular Biology

Background:

  • Natural killer (NK) cells are crucial for rapid antiviral responses.
  • IL-15 (Interleukin-15) has been considered essential for NK cell development, function, and survival.
  • Mice deficient in IL-15 exhibit significantly reduced NK cell populations.

Purpose of the Study:

  • To investigate NK cell responses during viral infection in the absence of IL-15 or common gamma signaling cytokines.
  • To determine if NK cells can proliferate and function independently of IL-15 during mouse cytomegalovirus (mCMV) infection.

Main Methods:

  • Infection of IL-15-deficient and IL-15Ralpha-deficient mice with mouse CMV (mCMV).
  • Analysis of NK cell populations, proliferation, cytokine secretion, and cytolytic function.
  • Assessment of NK cell responses in Rag2(-/-) x Il2rg(-/-) mice following mCMV infection.

Main Results:

  • Robust proliferation of functional Ly49H-bearing NK cells was observed in IL-15-deficient mice during mCMV infection.
  • Significant NK cell expansion (>300-fold) occurred in Rag2(-/-) x Il2rg(-/-) mice, dependent on m157 viral glycoprotein recognition and IL-12.
  • NK cells demonstrated cytokine secretion and cytolytic function despite the absence of IL-15 or common gamma signaling.

Conclusions:

  • NK cells exhibit a previously unrecognized independence from IL-15 and other common gamma signaling cytokines during viral infection.
  • Viral recognition and IL-12 signaling can drive NK cell expansion and effector functions in specific immune-deficient contexts.
  • These findings challenge established paradigms of NK cell homeostasis and antiviral immunity.

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