Department of Immunology, Institute for Biological Research Sinisa Stankovic, University of Belgrade, Bulevar Despota Stefana 142, 11108 Belgrade, Serbia.
Immunol Res. 2012 Apr;52(1-2):81-8. doi: 10.1007/s12026-012-8281-y.
During evolution, beta cells adapted to a sole aim: the production and stimulus-dependent secretion of insulin. This acquired specificity was accompanied by a loss of protection mechanisms predisposing beta cell to a high vulnerability. Among beta cell-damaging molecules, a new one has been identified recently: macrophage migration inhibitory factor (MIF). MIF was at first designated as a T-cell product that inhibits random movement of macrophages. Over the years, the number of functions attributed to this protein increased significantly, positioning MIF at the top of inflammatory cascade in the combat against infection and in immunoinflammatory and autoimmune diseases. This exceptionally versatile molecule regulates insulin secretion in physiological conditions, while in pathological states it alters beta cell function and induces their apoptosis or necrosis and affects beta cell neoplasia.
在进化过程中,β 细胞适应了一个唯一的目标:胰岛素的产生和刺激依赖性分泌。这种获得的特异性伴随着保护机制的丧失,使β细胞容易受到高度的脆弱性影响。在破坏β细胞的分子中,最近又发现了一种新的分子:巨噬细胞移动抑制因子(MIF)。MIF 最初被指定为一种 T 细胞产物,可抑制巨噬细胞的随机运动。多年来,赋予这种蛋白质的功能数量显著增加,使 MIF 在对抗感染以及免疫炎症和自身免疫性疾病的炎症级联反应中处于领先地位。这种非常灵活的分子在生理条件下调节胰岛素分泌,而在病理状态下,它改变β细胞的功能并诱导其凋亡或坏死,并影响β细胞肿瘤的发生。