Breach of IL-12 monopoly in the initiation of type 1 immunity to intracellular infections: IL-12 is not required

Cell Mol Biol (Noisy-le-grand). 2001 Jun;47(4):689-94.

Abstract

IL-12 is believed to play an important role in type 1 T-cell differentiation and type 1 cytokine IFN-gamma release by T- and NK-cells and macrophages in host defense against intracellular infections by bacteria, parasites, fungi and viruses. However, recent studies by us and others have provided unequivocal evidence that while IL- 12 is critically required for the development of type 1 immunity to the majority of intracellular bacterial, parasitic and fungal infections, it is not required for anti-viral type 1 immune responses. These findings have provoked our re-thinking about the role of IL-12 in type 1 immunity and the search for additional cytokines capable of initiating anti-viral type 1 immunity. We hypothesize that there exist multiple cytokines including IL-12 which play a redundant role in the initiation of type 1 immunity against viral infection. These cytokines are likely released from not only antigen-presenting macrophages/dendritic cells but many other cell types, which suits the mode of viral infection. The existence of multiple factors capable of driving type 1 immunity endows the host with additional safeguards to cope with prevalent viral foes.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Bacterial Infections / immunology
  • Humans
  • Influenza, Human / immunology
  • Interferon-gamma / biosynthesis
  • Interleukin-12 / immunology*
  • Lymphocytic Choriomeningitis / immunology
  • Mycoses / immunology
  • Parasitic Diseases / immunology
  • Th1 Cells / immunology*
  • Virus Diseases / immunology*

Substances

  • Interleukin-12
  • Interferon-gamma