Division of Nephrology and Endocrinology, Naval Medical Center of PLA, Naval Medical University, Shanghai, People's Republic of China.
Division of Nephrology, Departments of Medicine, Durham VA and Duke University Medical Center, Durham, North Carolina, USA.
Kidney Int. 2024 Apr;105(4):661-663. doi: 10.1016/j.kint.2024.01.014.
Autosomal dominant polycystic kidney disease (ADPKD) has long been considered a genetic renal disorder, but emerging evidence suggests that the immune microenvironment within the kidney plays a pivotal role in disease progression and severity. In recent years, the previously obscure cytokine interleukin-37 has proved a strong inhibitor of innate immunity in multiple disease models. However, its role in ADPKD has not received scrutiny. In a provocative study published in the current issue, Zylberberg et al. show that interleukin-37 activates interferon signaling in renal macrophages, which inhibits ADPKD initiation. This finding identifies interleukin-37 as a potential viable immunomodulatory therapy for ADPKD.
常染色体显性多囊肾病 (ADPKD) 一直被认为是一种遗传性肾脏疾病，但新出现的证据表明，肾脏内的免疫微环境在疾病进展和严重程度中起着关键作用。近年来，先前不为人知的细胞因子白细胞介素-37已被证明是多种疾病模型中固有免疫的强抑制剂。然而，其在 ADPKD 中的作用尚未受到关注。在本期发表的一项发人深省的研究中，Zylberberg 等人表明，白细胞介素-37激活了肾脏巨噬细胞中的干扰素信号，从而抑制了 ADPKD 的发生。这一发现将白细胞介素-37 确定为 ADPKD 潜在可行的免疫调节治疗方法。
