The inflammatory response is a complex, tightly regulated process activated by tissue wounding, foreign body invasion, and sterile inflammation. Over the decades, great progress has been made to advance our understanding of this process. One often overlooked aspect of inflammation is its sequel: resolution. We know that dysregulated resolution often results in numerous chronic degenerative diseases such as arthritis, cancer, and asthma. However, identification of components and mechanisms of resolving pathways lags behind those of proinflammatory processes, yet represents overlooked therapeutic opportunities. One approach is identification of endogenous, negative compensatory mechanisms, which are activated in response to inflammation for the purpose of resolution of that inflammatory stimuli. This review will focus on literature that describes expression and function of interleukin-19, a proposed anti-inflammatory cytokine, in numerous inflammatory diseases. The literature concerning IL-19 is complex, context-dependent, and often contradictory. The expression and function of IL-19 in the inflammatory response are in no way settled. We will attempt to clarify the role that this interesting and understudied cytokine plays in resolution of inflammation and discuss its mechanisms of action in different cell types. We will present a hypothesis that endogenous IL-19 expression in response to inflammatory stimuli is a cellular compensatory mechanism to dampen inflammation. We further present studies suggesting that while endogenously expressed IL-19 may be a response to inflammation, pharmacological levels may be necessary to effectively resolve the inflammatory cascade.

中文翻译：

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通过 IL-19 消除免疫和非免疫细胞中的炎症。

炎症反应是一个复杂的、严格调节的过程，由组织损伤、异物侵入和无菌炎症激活。几十年来，我们在加深对这一过程的理解方面取得了巨大进展。炎症经常被忽视的一个方面是其后果：消退。我们知道，解析失调通常会导致许多慢性退行性疾病，例如关节炎、癌症和哮喘。然而，对解决途径的成分和机制的识别落后于促炎症过程的成分和机制，但却代表了被忽视的治疗机会。一种方法是识别内源性负代偿机制，该机制响应炎症而被激活，以消除炎症刺激。本综述将重点关注描述白细胞介素 19（一种拟议的抗炎细胞因子）在多种炎症性疾病中的表达和功能的文献。有关 IL-19 的文献非常复杂、依赖于具体情况，而且常常相互矛盾。IL-19 在炎症反应中的表达和功能尚未确定。我们将尝试阐明这种有趣且尚未充分研究的细胞因子在炎症消退中所起的作用，并讨论其在不同细胞类型中的作用机制。我们将提出一个假设，即响应炎症刺激的内源性 IL-19 表达是抑制炎症的细胞补偿机制。我们进一步提出的研究表明，虽然内源表达的 IL-19 可能是对炎症的反应，但药理学水平可能是有效解决炎症级联反应所必需的。