免疫性血小板减少症与细胞因子谱之间的联系:通往新治疗靶点的桥梁

M. Andreescu
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摘要

免疫性血小板减少症(ITP)表现为血小板储备减少,主要是由于免疫介导的血小板破坏。ITP的发病机制复杂,涉及免疫系统的失调。本综述旨在总结ITP中细胞因子谱的现有知识及其对诊断、治疗和预后的潜在意义。一些研究报道,ITP患者的细胞因子谱与健康人不同。具体来说,有证据表明促炎因子(白细胞介素(IL)-6、肿瘤坏死因子(TNF)-α、干扰素(IFN)-γ)和抗炎因子(IL-10、TGF-β)失衡。ITP中的细胞因子谱似乎是异质性的,在不同的患者亚群中观察到不同的模式。例如,一些研究报道了th1型细胞因子谱,其特征是IFN-γ和TNF-α水平升高,而另一些研究报道了th2型细胞因子谱,其特征是IL-4和IL-10水平升高。也有证据表明,随着时间的推移,一些患者的细胞因子谱从Th1转变为Th2。ITP的细胞因子谱可能对诊断、治疗和预后有重要意义。靶向特定的细胞因子或细胞因子通路也可能是治疗ITP的一种有希望的方法。需要进一步的研究来更好地了解ITP中细胞因子谱的异质性及其对临床管理的潜在影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The link between immune thrombocytopenia and the cytokine profile: a bridge to new therapeutical targets
Immune thrombocytopenia (ITP) manifests as depleted platelet reserves, primarily due to the immune-mediated destruction of platelets. The pathogenesis of ITP is complex and involves dysregulation of the immune system. This review aimed to summarize the current knowledge of the cytokine profile in ITP and its potential implications for diagnosis, treatment, and prognosis. Several studies have reported that ITP patients have an altered cytokine profile from that of healthy individuals. Specifically, there is evidence of an imbalance of pro-inflammatory (interleukin (IL)-6, tumor necrosis factor (TNF)-α, interferon (IFN)-γ) and anti-inflammatory cytokines (IL-10, TGF-β). The cytokine profile in ITP appears to be heterogeneous, with different patterns observed in different subsets of patients. For example, some studies have reported a Th1-type cytokine profile, characterized by elevated levels of IFN-γ and TNF-α, while others have reported a Th2-type cytokine profile, characterized by elevated levels of IL-4 and IL-10. There is also evidence of a shift from a Th1 to a Th2 cytokine profile in some patients over time. The cytokine profile in ITP may have important implications for diagnosis, treatment, and prognosis. Targeting specific cytokines or cytokine pathways may also represent a promising therapeutic approach for ITP. Further studies are needed to better understand the heterogeneity of the cytokine profile in ITP and its potential implications for clinical management.
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