IL-22 increases the innate immunity of tissues

Immunity. 2004 Aug;21(2):241-54. doi: 10.1016/j.immuni.2004.07.007.

Abstract

Interleukin 22 (IL-22) is mainly produced by activated Th1 cells. The data presented here indicate that neither resting nor activated immune cells express IL-22 receptor, and IL-22 did not have any effects on these cells in vitro and in vivo. In contrast, cells of the skin and the digestive and respiratory systems represent putative targets of this cytokine. The expression of IL-22 receptor in keratinocytes was upregulated by Interferon-gamma. In these cells, IL-22 activated STAT3 and directly and transcriptionally increased the expression of beta-Defensin 2 and beta-Defensin 3. High levels of IL-22 were associated with strongly upregulated beta-Defensin expression in skin from patients with T cell-mediated dermatoses. Taken together, IL-22 does not serve the communication between immune cells but is a T cell mediator that directly promotes the innate, nonspecific immunity of tissues.

MeSH terms

  • Animals
  • DNA-Binding Proteins / immunology
  • DNA-Binding Proteins / metabolism
  • Humans
  • Immune System / immunology
  • Immune System / metabolism
  • Immunity, Innate / immunology
  • Immunity, Innate / physiology*
  • Interleukins / immunology
  • Interleukins / metabolism*
  • Keratinocytes / immunology
  • Keratinocytes / metabolism
  • Male
  • Mice
  • Receptors, Interleukin / immunology
  • Receptors, Interleukin / metabolism
  • STAT3 Transcription Factor
  • Skin / immunology
  • Skin / metabolism
  • Trans-Activators / immunology
  • Trans-Activators / metabolism
  • beta-Defensins / immunology
  • beta-Defensins / metabolism

Substances

  • DEFB103A protein, human
  • DEFB4A protein, human
  • DNA-Binding Proteins
  • Interleukins
  • Receptors, Interleukin
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • Stat3 protein, mouse
  • Trans-Activators
  • beta-Defensins
  • interleukin-22 receptor
  • interleukin-22