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首页> 美国卫生研究院文献>Journal of Dental Research >A New Inflammatory Cytokine on the Block: Re-thinking Periodontal Disease and the Th1/Th2 Paradigm in the Context of Th17 Cells and IL-17
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A New Inflammatory Cytokine on the Block: Re-thinking Periodontal Disease and the Th1/Th2 Paradigm in the Context of Th17 Cells and IL-17

机译：一种新型的炎性细胞因子：在Th17细胞和IL-17的背景下重新思考牙周疾病和Th1 / Th2范式

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For almost two decades, the Th1/Th2 paradigm has offered a productive conceptual framework for investigating the pathogenesis of periodontitis. However, as with many other inflammatory diseases, the observed role of T-cell-mediated immunity in periodontitis did not readily fit this model. A new subset of CD4+ T-cells was recently discovered that explains many of the discrepancies in the classic Th1/Th2 model, and has been termed “Th17” based on its secretion of the novel pro-inflammatory cytokine IL-17. The identification of Th17 cells as a novel effector T-cell population compels re-examination of periodontitis in the context of the new subset and its signature cytokines. This review aims to offer a clarifying insight into periodontal pathogenesis under the extended Th1/Th2/Th17 paradigm, and is predicated on the principle that periodontal disease activity is determined by a complex interplay between the immune system and periodontal pathogens. The re-examination of existing periodontal literature and further studies in the light of these new discoveries may help explain how the inflammatory response results in damage to the periodontium while generally failing to control the pathogens. This knowledge is essential for the development of immunomodulatory intervention strategies for fine-tuning the host response to maximize the protective and minimize the destructive aspects of the periodontal host response. Moreover, with the advent of anti-cytokine biologic drugs that target the Th1 and Th17 pathways in autoimmunity, the potential consequences to periodontal disease susceptibility in humans need to be understood.
机译：近二十年来，Th1 / Th2范式为研究牙周炎的发病机理提供了富有成效的概念框架。但是，与许多其他炎症性疾病一样，在牙周炎中观察到的T细胞介导的免疫作用并不容易适合该模型。最近发现了一个新的CD4 + T细胞子集，可以解释经典Th1 / Th2模型中的许多差异，并且由于其分泌的新型促炎细胞因子IL-17而被称为“ Th17”。在新的亚群及其标志性细胞因子的背景下，将Th17细胞鉴定为新型效应T细胞群体，迫使牙周炎的重新检查。这篇综述的目的是为在扩展的Th1 / Th2 / Th17范式下的牙周发病机理提供一个清晰的见解，其依据是牙周疾病的活动取决于免疫系统和牙周病原体之间复杂相互作用的原理。根据这些新发现，对现有牙周文献进行重新检查和进一步研究可能有助于解释炎症反应如何导致牙周膜受损，而通常无法控制病原体。该知识对于开发免疫调节干预策略至关重要，可用于微调宿主反应，以最大程度地保护和减少牙周宿主反应的破坏性方面。此外，随着针对自身免疫中针对Th1和Th17途径的抗细胞因子生物药物的问世，人们对人类牙周疾病易感性的潜在后果需要了解。

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