Tsuruta Daisuke
Department of Dermatology, Osaka City University Graduate School of Medicine, Asahimachi Abeno-ku, Osaka, Japan.
Recent Pat Inflamm Allergy Drug Discov. 2009 Jan;3(1):40-8. doi: 10.2174/187221309787158399.
Psoriasis is a common, chronic and relapsing autoimmune skin disease. Clinical characteristics of this disease are sharply-demarcated erythematous plaques covered with silver scales. Histologically, it is characterized by increased epidermal thickness, elongated papillae, and a moderate inflammatory infiltrate composed of lymphocytes, macrophages and neutrophils. The histological hallmark of psoriasis is Munro's microabscess, which is an accumulation of polymorphonuclear leukocytes in the keratinous layer. The mechanism of this disease is still an enigma, but genetic susceptibility, abnormal function of keratinocytes, or immunological disturbance, especially in T cells, are postulated. Over the past decades, there have been arguments about "keratinocyte-dependent" pathology as opposed to "immunocyte-dependent" pathology. Thus far, there have been some rodent models for psoriasis. Among them, the recent article from Rebholz et al. is quite intriguing because they explain the crosstalk between keratinocytes and lymphocytes: now evidence has been presented that while the aberrant NF-kappaB activation in either keratinocytes or lymphocytes could not reproduce psoriasis-like histology, such activation in both reproduced all of the aforementioned "hallmarks" of psoriasis pathology. Therefore, NF-kappaB may well act as a link between the T cell-mediated and keratinocyte-mediated arguments concerning the pathogenesis of psoriasis. This article also discusses some recent patent related to the field.
银屑病是一种常见的慢性复发性自身免疫性皮肤病。该疾病的临床特征为边界清晰的红斑鳞屑性斑块。组织学上，其特征为表皮增厚、乳头延长，以及由淋巴细胞、巨噬细胞和中性粒细胞组成的中度炎症浸润。银屑病的组织学标志是Munro微脓肿，即角质层中多形核白细胞的聚集。该疾病的发病机制仍是个谜，但推测与遗传易感性、角质形成细胞功能异常或免疫紊乱有关，尤其是T细胞。在过去几十年里，一直存在关于“角质形成细胞依赖性”病理与“免疫细胞依赖性”病理的争论。到目前为止，已经有一些银屑病的啮齿动物模型。其中，Rebholz等人最近的文章很有意思，因为他们解释了角质形成细胞和淋巴细胞之间的相互作用：现在有证据表明，虽然角质形成细胞或淋巴细胞中异常的NF-κB激活都不能重现银屑病样组织学表现，但两者同时激活则重现了银屑病病理的所有上述“特征”。因此，NF-κB很可能是T细胞介导和角质形成细胞介导的关于银屑病发病机制争论之间的一个联系。本文还讨论了该领域的一些近期专利。
