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首页> 外文期刊>Sarcoidosis, vasculitis, and diffuse lung diseases: official journal of WASOG >Cytokine and chemokine blockade as immunointervention strategy for the treatment of diffuse lung diseases.
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Cytokine and chemokine blockade as immunointervention strategy for the treatment of diffuse lung diseases.

机译：细胞因子和趋化因子阻断作为免疫干预策略，用于治疗弥漫性肺部疾病。

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Cytokines and chemokines are essential components for the pathophysiology of sarcoidosis. In the last decade, evidence has accumulated indicating that most of the events that lead to the alveolitis, granuloma formation and tissue injury are regulated by these mediators and their receptors. Recently, information on the possible pathogenetic role of cytokines has been translated into the development of potent cytokine antagonists which have proved to be powerful means of controlling disease activity in some inflammatory diseases. Molecules capable of neutralizing tumor necrosis factor-alpha (TNF-alpha) are currently used in the clinical setting of rheumatoid arthritis and active Crohn's disease. TNF-alpha is one of most important cytokines in the pathogenesis of sarcoidosis: not unexpectedly, data suggest the real possibility of using anti-TNF strategies to treat refractory sarcoidosis. These data are preliminary and should promote further clinical trials to confirm both the efficacy and tolerability of anti-TNF agents when used in patients with sarcoidosis and other interstitial lung diseases which are characterized by an up-regulation of TNF-alpha expression in the pulmonary milieu. Blockades of other inflammatory cytokines are also expected to be therapeutic in sarcoidosis and other T-cell mediated diffuse lung diseases. In particular, therapies directed at neutralizing chemokines and other molecules which control trafficking and accumulation of immunocompetent cells are potentially more selective and attractive but require a priori knowledge of precise pathways regulating the inflammation state involving the alveolar and interstitial structures.
机译：细胞因子和趋化因子是结节病病理生理学的重要组成部分。在过去的十年中，积累的证据表明，导致肺泡炎，肉芽肿形成和组织损伤的大多数事件都由这些介体及其受体调节。近来，关于细胞因子可能的致病作用的信息已被转化为有效的细胞因子拮抗剂的开发，其已被证明是控制某些炎性疾病中疾病活性的有效手段。能够中和肿瘤坏死因子-α（TNF-alpha）的分子目前用于类风湿关节炎和活动性克罗恩病的临床环境中。 TNF-α是结节病发病机理中最重要的细胞因子之一：并非意外，数据表明使用抗TNF策略治疗难治性结节病的真正可能性。这些数据是初步的，应进一步证实其用于结节病和其他以肺环境中的TNF-α表达上调为特征的其他间质性肺疾病的患者中抗TNF药物的耐受性的临床试验。其他炎性细胞因子的阻滞剂也有望在结节病和其他T细胞介导的弥漫性肺病中起到治疗作用。特别地，针对中和趋化因子和控制免疫活性细胞的运输和积累的其他分子的疗法可能更具选择性和吸引力，但需要先验知识来调节涉及肺泡和间质结构的炎症状态。

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