IL-12-deficient mice are defective but not devoid of type 1 cytokine responses

Ann N Y Acad Sci. 1996 Oct 31;795:60-70. doi: 10.1111/j.1749-6632.1996.tb52655.x.


Interleukin-12 (IL-12) has been described as a pivotal molecule in the immune response based in part on its ability to influence the differentiation of T helper (Th) cells into a type 1 (Th1) phenotype. This event is crucial in that appropriate differentiation of naive T cells can determine susceptibility or resistance to given pathogens by influencing the balance between cellular and humoral immunity. In order to further delineate the role of IL-12 in the immune response, we generated mice deficient for this cytokine. IL-12 knockout mice were viable, fully fertile, and displayed no obvious developmental abnormalities. Upon immunological analysis, these mice demonstrated an impaired ability to effect a Th1 response as well as an impaired ability to produce interferon-gamma in response to endotoxin in vivo. These data establish an essential role for IL-12 in the generation of optimal Th1 responses in vivo, but weak responses can occur independently of IL-12.

MeSH terms

  • Animals
  • Cytokines / physiology*
  • Interferon-gamma / biosynthesis
  • Interferon-gamma / physiology
  • Interleukin-12 / deficiency*
  • Lymphocyte Activation
  • Mice
  • Mice, Knockout
  • T-Lymphocyte Subsets
  • Th1 Cells / physiology*


  • Cytokines
  • Interleukin-12
  • Interferon-gamma