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Type 1 IFN-induced protein MxA and plasmacytoid dendritic cells in lesions of morphea

Mehran Ghoreishi1, Cristián Vera Kellet, Jan P Dutz

  • 1Department of Dermatology & Skin Science and Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada.

Experimental Dermatology
|April 18, 2012
PubMed

Insights

Type 1 interferons (IFN) may drive morphea, an autoimmune skin disease. Researchers found elevated MxA protein and plasmacytoid dendritic cells (pDCs) in morphea lesions, suggesting a role for type 1 IFN in disease pathogenesis.

Area of Science:

  • Immunodermatology
  • Autoimmune skin diseases
  • Fibrotic disorders

Background:

  • Morphea is an autoimmune sclerotic skin disease with unknown causes.
  • Type 1 interferons (IFN) are implicated in systemic sclerosis pathogenesis.
  • A potential role for type 1 IFN in morphea's inflammation and fibrosis is proposed.

Purpose of the Study:

  • To investigate the expression of type 1 IFN-inducible protein MxA and plasmacytoid dendritic cells (pDCs) in morphea lesions.
  • To compare these markers in morphea with other skin conditions like cutaneous lupus erythematosus, lichen planus, and keloid.
  • To compare lesional and non-lesional morphea skin.

Main Methods:

  • Immunohistochemistry was used to examine skin biopsies from 10 morphea patients.
  • Expression of MxA, CD123, and BDCA-2 (pDC markers) was assessed.
  • Comparisons were made between lesional and non-lesional morphea skin, and with other skin conditions.

Main Results:

  • MxA was expressed in the epidermis, reticular dermis, and subcutis of morphea lesions.
  • Plasmacytoid dendritic cells (pDCs) were abundant in morphea lesions, particularly around vessels and fibrous bundles.
  • Non-lesional morphea skin and keloid samples showed minimal to no expression of MxA and pDC markers.

Conclusions:

  • The study demonstrates the presence of type 1 IFN-related protein MxA and pDCs in lesional, but not non-lesional, morphea skin.
  • These findings suggest a potential role for type 1 interferons in the pathogenesis of morphea.
  • Further research into type 1 IFN pathways may offer new therapeutic targets for morphea.

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