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Limitations of current monoclonal antibodies for plaque-type psoriasis and an outlook for the future

机译：斑块型牛皮癣的当前单克隆抗体的限制和未来的前景

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Psoriasis is a chronic immune-mediated disease; although its pathogenesis is complex and still largely unknown, over the past several years, it has become clear that psoriasis goes beyond the skin. Improvements in our understanding of the pathogenesis have subsequently led to the development of novel drugs that act systemically on specific molecular components of the immune response [1]. Several cytokine pathways have been identified and investigated as targets for systemic therapies. Biologic agents have revolutionized the way to manage the psoriatic disease. They selectively inhibit cytokines associated with psoriatic plaque formation,such as tumor necrosis factor (TNF)-? interleukin (IL)-12/23, and IL-17A. Current consensus is that mild psoriasis can be effectively treated with topical agents, whereas systemic or biologic therapies are indicated for moderate to severe disease [1]. However, psoriasis at any severity grade can negatively impact on patients quality of life, thereby challenging the tag of mddisease. For this reason, in addition to body surface area affected and Psoriasis Area and Severity Index (PASI), other factors must be considered to evaluate treatment strategies, such as Dermatology Life Quality Index score and the burdens associated with symptoms of pain and itching [1]. An earlier use of biologics, targeting the underlying inflammation, may slow disease progression and prevent associated comorbidities, such as atherosclerosis and metabolic syndrome [2]. Patients affected by debilitating disease can now enjoy clear or almost-clear skin in most cases with biologic therapies. All biologics yield greater efficacy rates (PASI-75 responses ranging from 40% to 90%) with fewer adverse events and better overall tolerability when compared with conventional systemic therapies [3]. From a patient perspective, biologics seems to be aswonder drugs, nevertheless, they are not lacking of risks and limitations.
机译：牛皮癣是一种慢性免疫介导的疾病;虽然其发病机制是复杂的并且仍然很大程度上未知，但在过去几年中，它已经清楚地清楚地牛皮癣超越了皮肤。我们对发病机制的理解的改进随后导致了新型药物的开发，该药物系统在免疫反应的特定分子组分上全身性[1]。已经鉴定了几种细胞因子途径并被研究为全身疗法的靶标。生物制剂彻底改变了管理银屑病疾病的方式。它们选择性地抑制与银屑病斑块形成相关的细胞因子，例如肿瘤坏死因子（TNF） - ？白细胞介素（IL）-12/23和IL-17A。目前的共识是可以用局部药剂有效处理温和的牛皮癣，而全身或生物疗法表明中度至严重疾病[1]。然而，任何严重程度的牛皮癣都可以对患者的生活质量产生负面影响，从而挑战MDDisease的标签。因此，除了受影响和牛皮癣面积和严重程度指数（PASI）的身体表面积外，必须考虑其他因素来评估治疗策略，例如皮肤科生活质量指数评分和与疼痛症状相关的负担[1 ]。较早使用生物学，靶向潜在的炎症，可能会减缓疾病进展，并预防相关的合并症，如动脉粥样硬化和代谢综合征[2]。在大多数生物治疗的情况下，受衰弱疾病影响的患者现在可以在大多数情况下享受清晰或几乎清晰的皮肤。所有生物学均产生较高的疗效率（PASI-75响应从40％至90％的反应），与常规全身疗法相比，不良事件较少，更好的整体耐受性[3]。从患者的角度来看，生物学似乎是Aswonder药物，但它们并不缺乏风险和局限性。

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