Expression of the C-C chemokine MIP-3α/CCL20 in human epidermis with impaired permeability barrier function

被引:79
|
作者
Schmuth, M
Neyer, S
Rainer, C
Grassegger, A
Fritsch, P
Romani, N
Heufler, C
机构
[1] Univ Innsbruck, Dept Dermatol, A-6020 Innsbruck, Austria
[2] Univ Innsbruck, Dept Plast & Reconstruct Surg, A-6020 Innsbruck, Austria
关键词
barrier function; dendritic cells; stratum corneum; transepidermal water loss;
D O I
10.1034/j.1600-0625.2002.110205.x
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
External assault to the skin is followed by an epidermal response including synthesis of DNA, lipids, cytokines and migration of antigen presenting cells. MIP-3alpha (CCL20, LARC, Exodus-1, Scya20) is a recently described C-C chemokine, predominantly expressed in extralymphoid tissue, which is known to direct migration of dendritic cell precursors and memory lymphocytes to sites of antigen invasion. We assessed the expression of MIP-3a in human skin using semi-quantitative polymerase chain reaction. In vivo, MIP-3alpha mRNA was constitutively expressed at low levels in untreated human epidermis. After acute disruption of the epidermal permeabiltiy barrier MIP-3alpha mRNA was upregulated in the epidermal fraction, whereas dermal MIP-3alpha mRNA levels remained unchanged. In vitro, MIP-3alpha was increased in cultured keratinocytes treated with IL- 1alpha and TNF-alpha and was present in immature and mature dendritic cells, THP-1 monocytic cells and activated T cells. Finally, skin biopsies from patients with psoriasis, contact dermatitis and mycosis fungoides showed abundant expression. In biopsies from atopic dermatitis and graft vs. host disease a weak signal was present, whereas no expression was found in scleroderma and toxic epidermal necrolysis. We conclude that regulation of MIP-3alpha mRNA is part of the epidermal response to external assault. Its upregulation may represent a danger signal for increased inummosurveillance in barrier disrupted skin and inflammatory skin conditions with impaired barrier function to counteract potential antigen invasion.
引用
收藏
页码:135 / 142
页数:8
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