Laboratories of Cellular and Molecular Immunology, Division of Basic and Clinical Immunology, University of California, Irvine, CA 92697, USA.
J Clin Immunol. 2011 Jun;31(3):472-8. doi: 10.1007/s10875-010-9507-1. Epub 2011 Jan 18.
Leptin, one of the adipokines, functions as a hormone and a cytokine. In this investigation, we show for the first time that leptin, in a concentration-dependent manner, activates human peripheral blood B cells to induce secretion of IL-6, IL-10, and TNF-α. Leptin increased B cells expressing CD25 and HLA-DR. Leptin induces phosphorylation of Janus activation kinase 2 (JAK2), signal transducer and activator of transcription 3 (STAT3), p38 mitogen-activated protein kinase (p38MAPK), and extracellular signal-regulated kinase (ERK1/2). Furthermore, leptin-induced cytokine secretion by B cells was blocked by inhibitors of JAK2, STAT3, p38MAPK, and ERK1/2. These data demonstrate that leptin activates human B cells to secrete cytokines via activation of JAK2/STAT3 and p38MAPK/ERK1/2 signaling pathways, which may contribute to its inflammatory and immunoregulatory properties.
瘦素是脂肪细胞因子之一，具有激素和细胞因子的功能。在本研究中，我们首次表明，瘦素以浓度依赖的方式激活人外周血 B 细胞，诱导白细胞介素 6（IL-6）、白细胞介素 10（IL-10）和肿瘤坏死因子-α（TNF-α）的分泌。瘦素增加了表达 CD25 和 HLA-DR 的 B 细胞。瘦素诱导 Janus 激活激酶 2（JAK2）、信号转导和转录激活因子 3（STAT3）、丝裂原活化蛋白激酶 p38（p38MAPK）和细胞外信号调节激酶 1/2（ERK1/2）的磷酸化。此外，瘦素诱导的 B 细胞细胞因子分泌被 JAK2、STAT3、p38MAPK 和 ERK1/2 的抑制剂阻断。这些数据表明，瘦素通过激活 JAK2/STAT3 和 p38MAPK/ERK1/2 信号通路激活人 B 细胞分泌细胞因子，这可能有助于其炎症和免疫调节特性。
Zotero 插件
