标题： 银屑病通过密度型数学模型的免疫病理发生机制 显示英文标题

标题： Immunopathogenesis in Psoriasis through a Density-type Mathematical Model

摘要： 银屑病是一种慢性皮肤炎症，在皮肤表面表现为鳞状红斑病变。 几种免疫抑制药物的出现证实了该疾病源于人体血液中的免疫病理异常。 对该疾病的细胞生物学和临床研究显示，负责人体免疫的辅助T细胞和其他白细胞，如果在靠近真皮区域的位置大量产生，可能会导致银屑病的发生。 研究结果还表明，一个复杂的、自我维持的（细胞因子及相关）蛋白质网络在疾病发展过程中起着重要作用，实际上导致表皮角质形成细胞的大量增殖。 疾病的发生与这种过度增殖有关，导致皮肤表面脱落（银屑病斑块）。 通过复杂的生化反应链，增殖的角质形成细胞过量生成一氧化氮，这是银屑病斑块鳞片状特征的原因。 考虑到这些免疫病理机制，我们提出并分析了一个用于银屑病的数学时间微分模型。 分析结果与现有的细胞生物学和临床发现一致，并有一些新的预测，这些预测可以进一步进行验证。 显示英文摘要

摘要： Disease psoriasis occurs as chronic inflammation of skin and appears as scaly red lesions on skin surface. Advent of several immunosuppressive drugs established that the disease stems from immuno-pathogenic disorder in human blood. Cell biological as well as clinical research on the disease reveals that the helper T-cells and other Leucocytes, responsible for human immunity, may lead to psoriasis pathogenesis if produced in plenty at locations close to the dermal region. Research findings also showed that a complex, self-sustaining (cytokine and related) proteins network play important role in disease maturation by actually leading to a huge proliferation of epidermal keratinocytes. Disease pathogenesis is identified with such hyperproliferation leading to flaking of skin surface (psoriatic plaques). An excessive generation of nitric oxide by proliferated keratinocytes, through a complex chain of bio-chemical events, is causal to the scaliness of psoriatic plaques. Considering these immunopathogenic mechanisms, we propose and analyse a mathematical time differential model for the disease psoriasis. Outcomes of analysis are consistent with existing cell biological and clinical findings with some new predictions which could be tested further.