Differentiated keratinocytes are responsible for TNF-alpha regulated production of macrophage inflammatory protein 3alpha/CCL20, a potent chemokine for Langerhans cells

J Dermatol Sci. 2001 Oct;27(2):130-9. doi: 10.1016/s0923-1811(01)00127-x.

Abstract

The recruitment of immature dendritic cells into the epidermis is a key step in the development of cutaneous immunity, although the mechanism remains to be clarified. Recently, it was reported that both macrophage inflammatory protein 3alpha (MIP-3alpha)/CCL20 produced by keratinocytes and TNF-alpha are important in recruiting Langerhans cells (LC) to the epidermis. In this study, we examined the production of MIP-3alpha by human keratinocytes stimulated with TNF-alpha. Cultured keratinocytes showed enhanced expression of MIP-3alpha mRNA and protein when stimulated with TNF-alpha. In addition, conditioned medium from TNF-alpha-stimulated keratinocyte cultures induced the migration of L1.2 cells expressing CCR6. We next examined the production of MIP-3alpha in stratified keratinocytes and found that, in contrast to non-stratified keratinocytes, stimulation with TNF-alpha increased the expression of MIP-3alpha mRNA and protein. Moreover, skin samples grown in organ culture and treated with TNF-alpha showed MIP-3alpha in the keratinocytes of the spinous layer, but not in the basal layer, by immunofluorescence staining. Based on these results, we postulate that MIP-3alpha produced by keratinocytes in the spinous layer in response to TNF-alpha stimulation is a key chemokine responsible for the epidermal recruitment of Langerhans cells.

MeSH terms

  • Cell Differentiation
  • Cells, Cultured
  • Chemokine CCL20
  • Chemokines, CC / genetics*
  • Chemotaxis / drug effects
  • Chemotaxis / physiology
  • Gene Expression Regulation / drug effects*
  • Humans
  • Keratinocytes / cytology
  • Keratinocytes / drug effects
  • Keratinocytes / physiology*
  • Macrophage Inflammatory Proteins / genetics*
  • Organ Culture Techniques
  • RNA, Messenger / genetics
  • Receptors, CCR6
  • Receptors, Chemokine*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Skin / cytology*
  • Skin / drug effects
  • Skin Physiological Phenomena*
  • Transcription, Genetic / drug effects*
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • CCL20 protein, human
  • CCR6 protein, human
  • Chemokine CCL20
  • Chemokines, CC
  • Macrophage Inflammatory Proteins
  • RNA, Messenger
  • Receptors, CCR6
  • Receptors, Chemokine
  • Tumor Necrosis Factor-alpha