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首页> 外文期刊>Rheumatology international. >The role of interleukin-23/interleukin-17 axis in the development of systemic lupus erythematosus among patients with tuberculosis: Comment on: Lin YC, Liang SJ, Liu YH et al.: Tuberculosis as a risk factor for systemic lupus erythematosus: Results of a nationwide study in Taiwan. (Rheumatol Int. 2011 Mar 18. [Epub ahead of print])
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The role of interleukin-23/interleukin-17 axis in the development of systemic lupus erythematosus among patients with tuberculosis: Comment on: Lin YC, Liang SJ, Liu YH et al.: Tuberculosis as a risk factor for systemic lupus erythematosus: Results of a nationwide study in Taiwan. (Rheumatol Int. 2011 Mar 18. [Epub ahead of print])

机译：白细胞介素-23 /白介素17轴在结核病患者系统性红斑狼疮发展中的作用：评论：Lin YC，Liang SJ，Liu YH et al .:结核病是系统性红斑狼疮的危险因素：台湾的全国性研究（Rheumatol Int。2011年3月18日。[Epub提前发行]）

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We read with great interest the contribution by Lin et al. [1]. They evaluated the relationship between Mycobacte-rium tuberculosis (TB) and systemic lupus erythematosus (SLE) and reported an increased risk of precipitating SLE among patients with TB (P < 0.0001). However, they did not explicate the exact mechanism. We would like to suggest a possible pathomechanism of SLE in patients with TB. During primary TB, interferon (IFN)-y, produced by CD4(+) T helper (Th) 1 cells, and interleukin (IL)-17, largely produced by Thl7 cells and suppressed by IFN-gamma, are induced [2]. Both IFN-gama and IL-17 promote cell recruitment and granuloma organization throughout infection [2]. However, dysregulated balance of Thl and Thl7 cells, as a shift of the response toward excessive IL-17, sustains extensive neutrophil recruitment and tissue damage during the chronic phase of primary TB [2, 3]. Both the IL-17 and the Thl7 response to TB are dependent upon IL-23.
机译：我们非常感兴趣地阅读了Lin等人的文章。 [1]。他们评估了结核分枝杆菌（TB）与系统性红斑狼疮（SLE）之间的关系，并报告了结核病患者发生SLE的风险增加（P <0.0001）。但是，他们没有阐明确切的机制。我们想建议结核病患者可能发生SLE。在原发性结核病期间，诱导了CD4（+）T辅助（Th）1细胞产生的干扰素（IFN）-y和Thl7细胞大量产生且被IFN-γ抑制的白介素（IL）-17 [2]。 。在整个感染过程中，IFN-γ和IL-17均可促进细胞募集和肉芽肿组织[2]。然而，在原发性结核的慢性期，随着反应向过度的IL-17转移，Th1和Th17细胞的平衡失调维持了广泛的嗜中性白细胞募集和组织损伤[2，3]。 IL-17和Thl7对结核病的反应均取决于IL-23。

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