Farrell A M, Marren P, Dean D, Wojnarowska F
Department of Dermatology, Churchill Hospital, Headington, Oxford OX2 8LQ, U.K.
Br J Dermatol. 1999 Jun;140(6):1087-92.
An immunohistochemical approach was used to characterize the inflammatory infiltrate in vulval lichen sclerosus, using monoclonal antibodies to CD3, CD4, CD8, CD68 and HLA-DR. Significant numbers of CD4 + and CD8 + lymphocytes were observed in the dermal band of inflammatory cells in approximately equal proportions. Less numerous CD4 + and CD8 + lymphocytes also occurred adjacent to the dermoepidermal junction and occasionally in the lower epidermis. Increased numbers of cells staining with the monocyte/macrophage marker CD68 were also present in the band of inflammatory cells as well as being scattered diffusely throughout the sclerotic region. Expression of HLA-DR in the lichen sclerosus specimens was increased within the inflammatory infiltrate and around blood vessels in the dermis. All the vulval lichen sclerosus specimens also demonstrated some HLA-DR expression around the keratinocytes, suggesting that these keratinocytes might be involved in antigen presentation. We also studied the expression of CD44 and its isoforms 3G5 (marker of V3), 8G5 (marker of V6), 3D2 (marker of V4/5) and IE8 (marker of V8/9). CD44 has been proposed to play a part in lymphocyte homing, cell-matrix interaction (particularly with hyaluronic acid), lymphocyte activation and malignant progression of certain tumours. The epidermis of the lichen sclerosus specimens appeared to demonstrate a greater intensity of staining with the pan-CD44 marker F10-44, and reduced staining with 3G5, 3D2 and IE8 compared with normal skin. Like normal skin, the dermis of the lichen sclerosus specimens did not demonstrate staining with 3G5, 3D2, 8G5 or 1E8, but did show staining with F10-44. However, the pattern of the dermal staining with F10-44 reflected the position of the inflammatory infiltrate and was sparse in the five sections where there was a prominent sclerotic zone, but increased in the three sections where there was a prominent band of inflammation cells. Our results demonstrate evidence of immunological changes at all levels of skin involved by lichen sclerosus, including the epidermis.
采用免疫组织化学方法，使用针对CD3、CD4、CD8、CD68和HLA - DR的单克隆抗体来表征外阴硬化性苔藓中的炎性浸润。在炎性细胞的真皮带中观察到大量CD4⁺和CD8⁺淋巴细胞，比例大致相等。在真皮表皮交界处附近也有较少数量的CD4⁺和CD8⁺淋巴细胞，偶尔在表皮下层也有。用单核细胞/巨噬细胞标志物CD68染色的细胞数量增加，这些细胞既存在于炎性细胞带中，也分散在整个硬化区域。硬化性苔藓标本中HLA - DR在炎性浸润内和真皮血管周围的表达增加。所有外阴硬化性苔藓标本在角质形成细胞周围也显示出一些HLA - DR表达，这表明这些角质形成细胞可能参与抗原呈递。我们还研究了CD44及其异构体3G5（V3标志物）、8G5（V6标志物）、3D2（V4/5标志物）和IE8（V8/9标志物） 的表达。有人提出CD44在淋巴细胞归巢、细胞 - 基质相互作用（特别是与透明质酸）、淋巴细胞活化和某些肿瘤的恶性进展中起作用。与正常皮肤相比，硬化性苔藓标本的表皮似乎用泛CD44标志物F10 - 44染色强度更大，而用3G5、3D2和IE8染色减少。与正常皮肤一样，硬化性苔藓标本的真皮未显示用3G5、3D2、8G5或1E8染色，但显示用F10 - 44染色。然而，F10 - 44的真皮染色模式反映了炎性浸润的位置，在有明显硬化区的五个切片中稀疏，但在有明显炎性细胞带的三个切片中增加。我们的结果证明了硬化性苔藓累及的皮肤各层包括表皮存在免疫变化的证据。
