Boehncke W H, Sterry W, Hainzl A, Scheffold W, Kaufmann R
Department of Dermatology, University of Ulm, Germany.
Arch Dermatol Res. 1994;286(6):325-30. doi: 10.1007/BF00402223.
Preliminary observations in a xenogeneic SCID mouse transplantation model indicated that murine epidermis overgrows human dermis from psoriatic skin but not that form normal skin. To investigate the effect of peripheral blood mononuclear cells on the differentiation of murine keratinocytes, we transplanted involved and uninvolved full-thickness skin from patients with psoriasis onto SCID mice and followed this with repeated subcutaneous injections of cells suspended in patient serum. After 6 weeks grafts were analysed morphologically and immunohistochemically. The epidermis in grafts from clinically uninvolved skin appeared normal. The persistence of a psoriasiform epidermis was noted in all grafts from affected sites despite a lack of lymphocytic infiltration. Staining for human and mouse MHC class I antigens revealed the murine origin of keratinocytes forming the psoriasiform epidermis, while the human dermis was retained. Our observations indicate that the defect underlying the pathogenesis of psoriasis is most likely located in the dermal rather than the epidermal compartment. This xenogeneic transplantation model may be useful for future studies of the pathogenesis and treatment of psoriasis.
在一个异种SCID小鼠移植模型中的初步观察表明,来自银屑病皮肤的人真皮上生长的是鼠表皮,而来自正常皮肤的则不是。为了研究外周血单核细胞对鼠角质形成细胞分化的影响,我们将银屑病患者的病变和非病变全层皮肤移植到SCID小鼠上,随后反复皮下注射悬浮在患者血清中的细胞。6周后,对移植物进行形态学和免疫组织化学分析。来自临床非病变皮肤的移植物中的表皮看起来正常。尽管缺乏淋巴细胞浸润,但在所有来自病变部位的移植物中都观察到了银屑病样表皮的持续存在。对人和小鼠MHC I类抗原的染色显示,形成银屑病样表皮的角质形成细胞起源于小鼠,而人真皮得以保留。我们的观察表明,银屑病发病机制的潜在缺陷很可能位于真皮而非表皮部分。这种异种移植模型可能对未来银屑病发病机制和治疗的研究有用。