Hansen E R, Vejlsgaard G L, Lisby S, Heidenheim M, Baadsgaard O
Department of Dermatology, Rigshospitalet, Copenhagen, Denmark.
J Invest Dermatol. 1991 Nov;97(5):818-23. doi: 10.1111/1523-1747.ep12489011.
Previous studies have suggested that epidermal-derived interleukin-1 is involved in the pathogenesis of cutaneous T-cell lymphoma (CTCL); however, the findings are conflicting and studies that combine immunohistochemistry and functional activity have not been performed. We investigated the interleukin-1 level in epidermis of patients with cutaneous T-cell lymphoma using both immunohistochemistry, enzyme-linked immunosorbent assays, and the thymocyte co-stimulation assay. Using supernatants obtained from epidermal cell cultures, we found a significant but small increase of interleukin 1 alpha protein release from involved CTCL epidermis compared to normal epidermis from healthy individuals. Both keratinocytes and leukocytes could release interleukin-1 alpha, but the majority was derived from the keratinocytes. Interleukin-1 beta protein was not detectable. In the thymocyte assay, interleukin-1 alpha was found to be biologically active. When lymphokines derived from a T-cell clone obtained from involved CTCL skin were co-cultured with epidermal cells, an enhanced release of epidermal interleukin-1 alpha could be demonstrated. Because interleukin 1 alpha was increased, we investigated the presence of interleukin 1-inducible keratinocyte-derived interleukin 8 and found it increased in CTCL epidermis compared to normal epidermis from healthy individuals. This study demonstrated an elevated epidermal IL-1 alpha level and IL-8 immunoreactivity in CTCL epidermis, which suggests that this elevated level is induced by lymphokines released from activated T cells.
先前的研究表明，表皮来源的白细胞介素-1参与皮肤T细胞淋巴瘤（CTCL）的发病机制；然而，研究结果相互矛盾，且尚未开展结合免疫组织化学和功能活性的研究。我们使用免疫组织化学、酶联免疫吸附测定法和胸腺细胞共刺激测定法，对皮肤T细胞淋巴瘤患者表皮中的白细胞介素-1水平进行了研究。利用从表皮细胞培养物中获得的上清液，我们发现，与健康个体的正常表皮相比，受累CTCL表皮中白细胞介素1α蛋白的释放有显著但微小的增加。角质形成细胞和白细胞均可释放白细胞介素-1α，但大部分来自角质形成细胞。未检测到白细胞介素-1β蛋白。在胸腺细胞测定中，发现白细胞介素-1α具有生物活性。当将来自受累CTCL皮肤的T细胞克隆产生的淋巴因子与表皮细胞共同培养时，可证明表皮白细胞介素-1α的释放增加。由于白细胞介素1α增加，我们研究了白细胞介素1诱导的角质形成细胞来源的白细胞介素8的存在情况，发现与健康个体的正常表皮相比，CTCL表皮中的该物质增加。这项研究表明，CTCL表皮中表皮白细胞介素-1α水平和白细胞介素-8免疫反应性升高，这表明这种升高水平是由活化T细胞释放的淋巴因子诱导的。
