In the absence of IL-12, CD4(+) T cell responses to intracellular pathogens fail to default to a Th2 pattern and are host protective in an IL-10(-/-) setting

Immunity. 2002 Mar;16(3):429-39. doi: 10.1016/s1074-7613(02)00278-9.


IL-12-deficient mice exposed to nonlethal infections with intracellular pathogens or repeatedly immunized with a pathogen extract developed lowered but nevertheless substantial numbers of IFN-gamma(+) CD4(+) T cells compared to those observed in wild-type animals. Moreover, the CD4(+) responses in these knockout animals failed to default to a Th2 pattern. The protective efficacy of the Th1 cells developing in an IL-12-deficient setting was found to be limited by IL-10 since mice doubly deficient in IL-10 and IL-12 survived, while animals deficient in IL-12 alone succumbed to pathogen challenge. In contrast to IL-12 knockout mice, MyD88-deficient animals exposed to a Th1 microbial stimulus developed a pure Th2 response, arguing that this signaling element plays a more critical function than IL-12 in determining pathogen-induced CD4 polarization.

MeSH terms

  • Adaptor Proteins, Signal Transducing
  • Animals
  • Antigens, Differentiation / genetics
  • Antigens, Differentiation / immunology
  • CD4-Positive T-Lymphocytes / immunology*
  • Immunity, Innate*
  • Interleukin-10 / genetics
  • Interleukin-10 / immunology*
  • Interleukin-12 / genetics
  • Interleukin-12 / immunology*
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Myeloid Differentiation Factor 88
  • Receptors, Immunologic / genetics
  • Receptors, Immunologic / immunology
  • Signal Transduction / immunology
  • Th1 Cells / immunology*
  • Th2 Cells / immunology*


  • Adaptor Proteins, Signal Transducing
  • Antigens, Differentiation
  • Myd88 protein, mouse
  • Myeloid Differentiation Factor 88
  • Receptors, Immunologic
  • Interleukin-10
  • Interleukin-12