From innate to adaptive immune responses in contact hypersensitivity

Curr Opin Allergy Clin Immunol. 2008 Aug;8(4):289-93. doi: 10.1097/ACI.0b013e3283088cf9.

Abstract

Purpose of review: To summarize recent findings that highlight the importance of the innate inflammatory immune responses in contact dermatitis and their role for the adaptive T-cell response to contact allergens. Implications for anti-inflammatory therapy based on recent reports are discussed.

Recent findings: Allergic contact dermatitis is studied widely in the mouse model. Recent work has identified an important role of innate pattern recognition receptors and innate immune cells in contact hypersensitivity. The role of skin dendritic cells has been studied with novel approaches for in-vivo depletion. New findings were made in the field of anti-inflammatory therapy either by uncovering new aspects of pathomechanisms or by the use of drugs that target different elements of the inflammatory cascade.

Summary: Inflammation is a pivotal element of allergic contact dermatitis. Studies in the mouse contact hypersensitivity model are beginning to shed light on the still largely unknown molecular mechanisms that enable contact allergens such as chemicals, metal ions and plant compounds to initiate the inflammatory innate immune response. This is a prerequisite for the adaptive immune response to occur. The recent progress in research points out the great potential of anti-inflammatory therapy covering a wide range of molecular targets.

Publication types

  • Review

MeSH terms

  • Animals
  • Cannabinoid Receptor Modulators / immunology
  • Dermatitis, Contact / immunology*
  • Dermatitis, Contact / physiopathology
  • Dermatitis, Contact / therapy
  • Humans
  • Immunity, Cellular*
  • Immunity, Innate*
  • Immunotherapy
  • Langerhans Cells / immunology
  • Langerhans Cells / metabolism
  • Langerhans Cells / pathology
  • Mice
  • Toll-Like Receptors / immunology*
  • Toll-Like Receptors / metabolism

Substances

  • Cannabinoid Receptor Modulators
  • Toll-Like Receptors