Volc-Platzer B, Rappersberger K, Mosberger I, Hinterberger W, Emminger-Schmidmeier W, Radaszkiewicz T, Wolff K
Department of Dermatology I, University of Vienna, Austria.
J Invest Dermatol. 1988 Aug;91(2):162-8. doi: 10.1111/1523-1747.ep12464407.
Graft-vs-host disease is generally viewed as an immunologically mediated disease. In search of additional tools for early diagnosis and an elucidation of the pathogenic mechanisms we investigated the expression kinetics of hemopoietic differentiation and class II alloantigens on both resident and passenger skin cells after bone marrow transplantation. HLA-DR antigens, which are found normally on the dendritic epidermal Langerhans cells only, are synthesized and expressed by keratinocytes within lesions of acute and chronic cutaneous graft-vs-host disease. Within non-lesional skin, however, during the course of cutaneous graft-vs-host eruptions, no clear cut expression of keratinocyte-bound HLA-DR antigens can be identified, suggesting that this phenomenon is locally restricted rather than generalized. Furthermore, our data indicate that within lesions clinically suggestive of cutaneous graft-vs-host disease but lacking diagnostic histopathologic criteria, KC-bound HLA-DR antigens can be readily identified. The second class II alloantigens investigated within the epidermis, the HLA-DQ antigens, were seen on Langerhans cells only and were not or only rarely detectable on keratinocytes. Several subtypes of CD3+ T lymphocytes were present in the epidermis of acute graft-versus-host lesions: one portion of CD3+ T lymphocytes also displayed the CD8 antigen; one portion, mainly localized within the basal layer, displayed the CD8 and/or the CD4 antigen; and one portion did not allow identification of CD8, CD4, or Leu7 antigens. In chronic cutaneous graft-versus-host lesions CD3+/CD8+ T lymphocytes predominated. CD1+ epidermal Langerhans cells were reduced in number and appeared rounded with blunt dendrites both in acute and chronic cutaneous graft-vs-host disease, but also, though to a lesser extent, within normal appearing skin from bone marrow transplanted patients without cutaneous graft-vs-host disease.
移植物抗宿主病通常被视为一种免疫介导性疾病。为了寻找早期诊断的额外工具并阐明其致病机制，我们研究了骨髓移植后驻留和过客皮肤细胞上造血分化和II类同种异体抗原的表达动力学。HLA - DR抗原通常仅在树突状表皮朗格汉斯细胞上发现，在急性和慢性皮肤移植物抗宿主病的病变中由角质形成细胞合成并表达。然而，在非病变皮肤中，在皮肤移植物抗宿主疹发作过程中，无法识别角质形成细胞结合的HLA - DR抗原的明确表达，这表明这种现象是局部受限而非全身性的。此外，我们的数据表明，在临床上提示皮肤移植物抗宿主病但缺乏诊断性组织病理学标准的病变中，可以很容易地识别角质形成细胞结合的HLA - DR抗原。在表皮中研究的第二类II类同种异体抗原，即HLA - DQ抗原，仅在朗格汉斯细胞上可见，在角质形成细胞上未检测到或仅很少检测到。急性移植物抗宿主病变的表皮中有几种CD3 + T淋巴细胞亚型：一部分CD3 + T淋巴细胞也表达CD8抗原；一部分主要位于基底层，表达CD8和/或CD4抗原；还有一部分无法识别CD8、CD4或Leu7抗原。在慢性皮肤移植物抗宿主病变中，CD3 + / CD8 + T淋巴细胞占主导。在急性和慢性皮肤移植物抗宿主病中，CD1 + 表皮朗格汉斯细胞数量减少，呈圆形，树突钝圆，不过在没有皮肤移植物抗宿主病的骨髓移植患者外观正常的皮肤中也有减少，只是程度较轻。
