Immune thrombocytopenia (ITP) is an autoimmune disorder characterized by autoimmune-mediated platelet destruction and impaired platelet production, which can lead to an increased risk of bleeding. The clinical management of ITP currently remains a challenge for hematologists. We explored the role of interleukin-9 (IL-9) in the treatment of CD41-induced ITP, and investigated its underlying mechanisms in a CD41-induced ITP mouse model. IL-9 treatment increased the numbers of mature megakaryocytes (CD41+CD42d+) and CD41+Sca-1+ cells in the bone marrow in these model mice, while IL-9 receptor (IL-9R) small interfering RNA (siRNA) inhibited the process. Moreover, phosphorylated signal transducer and activator of transcription 5 (STAT5), as a downstream molecule of IL-9R, was increased after IL-9 treatment. We next investigated the source of IL-9 in bone marrow, osteoblasts produced the highest level of IL-9. These results confirmed that IL-9 could prevent CD41-induced ITP in BALB/c mice by regulating osteoblasts and activating IL-9R/STAT5 signaling in megakaryocytes, thus providing further evidence for IL-9 as a promising therapeutic agent for the treatment of ITP.

中文翻译：

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白介素9通过JAK / STAT5信号传导防止小鼠免疫性血小板减少。

免疫性血小板减少症（ITP）是一种自身免疫性疾病，其特征是自身免疫介导的血小板破坏和血小板生成受损，这可能导致出血风险增加。目前，ITP的临床管理仍然是血液学家的一项挑战。我们探讨了白介素9（IL-9）在治疗CD41诱导的ITP中的作用，并研究了其在CD41诱导的ITP小鼠模型中的潜在机制。IL-9治疗可增加这些模型小鼠骨髓中成熟的巨核细胞（CD41 + CD42d +）和CD41 + Sca-1 +细胞的数量，而IL-9受体（IL-9R）小干扰RNA（siRNA）则抑制了这种表达。过程。此外，IL-9处理后，作为IL-9R的下游分子的磷酸化信号转导子和转录激活因子5（STAT5）增加了。接下来，我们调查了骨髓中IL-9的来源，成骨细胞产生了最高水平的IL-9。这些结果证实，IL-9可以通过调节成骨细胞和激活巨核细胞中的IL-9R / STAT5信号传导来预防CD41诱导的BALB / c小鼠的ITP，从而为IL-9作为治疗ITP的有希望的治疗剂提供了进一步的证据。 。