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在狼性炎的发病过程中,细胞介质素-23受体信号传递

Rong Fu¹, Afroditi Boulougoura¹, Shuilian Yu¹

¹Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.

Arthritis & rheumatology (Hoboken, N.J.)

|September 15, 2025

概括

介素-23受体 (IL-23R) 在狼性炎中被上调,从而损害受体细胞. 针对易患狼的小鼠的皮囊细胞中的IL-23R预防了淋巴结核炎的发展,提供了潜在的治疗策略.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
免疫学免疫学免疫学
细胞生物学细胞生物学

背景情况:

介质素-23 (IL-23) 在狼性炎 (LN) 中升高,但其在细胞损伤中的具体作用尚不清楚.
细胞对于脏过至关重要,它们的损伤是丸炎的标志.

研究的目的:

为了研究IL-23对细胞的影响.
在小鼠模型中,确定阻断 podocytes 中的 IL-23 受体 (IL-23R) 是否可以预防狼性炎.

主要方法:

在人类狼性炎脏活检中对IL-23R进行免疫组织化学染色.
在实验室研究中,使用人体和小鼠受IL-23刺激的受体细胞.
大量RNA测序IL-23-刺激的人类受体细胞.
产生容易患有狼的小鼠,具有 podocyte 特定的 Il23r. 删除.

主要成果:

在狼性腎炎患者的膠質細胞和在IL-23刺激后的 podocytes 中,IL-23R的表達顯著增加.
激发IL-23导致人体皮细胞中的synaptopodin表达减少和actin细胞骨架重塑.
带有 podocyte 特定 Il23r 缺失的小鼠表现出狼性炎的临床和组织学迹象减少.

结论:

在狼性腎炎的 podocytes 中,IL-23R 是上調的.
IL-23的信号传递会破坏细胞底细胞的结构和功能,从而导致质核突炎.
准 podocyte IL-23R 消除了小鼠狼性炎的发展,这表明了治疗目标.

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