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IL-21 limits NK cell responses and promotes antigen-specific T cell activation: a mediator of the transition from innate to adaptive immunity.

IFNalpha/beta, IL-12, and IL-15 regulate NK cell activation and expansion, but signals triggering resolution of the NK response upon induction of adaptive immunity remain to be defined. We now report that IL-21, a product of activated T cells, may serve this function. Mice lacking IL-21R (IL-21R(-/-)) had normal NK cell development but no detectable responses to IL-21. IL-21 enhanced cytotoxic activity and IFNgamma production by activated murine NK cells but did not support their viability, thus limiting their duration of activation. Furthermore, IL-21 blocked IL-15-induced expansion of resting NK cells, thus preventing the initiation of further innate responses. In contrast, IL-21 enhanced the proliferation, IFNgamma production, and cytotoxic function of CD8(+) effector T cells in an allogeneic MLR. These observations suggest that IL-21 promotes the transition between innate and adaptive immunity.

Pubmed ID: 11970879


  • Kasaian MT
  • Whitters MJ
  • Carter LL
  • Lowe LD
  • Jussif JM
  • Deng B
  • Johnson KA
  • Witek JS
  • Senices M
  • Konz RF
  • Wurster AL
  • Donaldson DD
  • Collins M
  • Young DA
  • Grusby MJ



Publication Data

April 23, 2002

Associated Grants

  • Agency: NIAID NIH HHS, Id: AI 40171

Mesh Terms

  • Animals
  • Antigens, CD44
  • Apoptosis
  • CD8-Positive T-Lymphocytes
  • Cytotoxicity, Immunologic
  • Female
  • Immunity, Active
  • Immunity, Innate
  • Interleukin-15
  • Interleukin-21 Receptor alpha Subunit
  • Interleukins
  • Isoantigens
  • Killer Cells, Natural
  • Lymphocyte Activation
  • Lymphocyte Count
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Receptors, Interleukin
  • Receptors, Interleukin-2
  • Receptors, Interleukin-21