Kudrin Alex, Ray David
Centre for Molecular Medicine, University of Manchester, Manchester, UK.
Immunol Cell Biol. 2008 Mar-Apr;86(3):232-8. doi: 10.1038/sj.icb.7100133. Epub 2007 Nov 27.
Macrophage migration inhibitory factor (MIF) has an amazing history of rediscoveries and controversies surroundings its true biological function. It has been classified as a powerful cytokine capable of inducing tumour necrosis factor (TNF)-alpha, IL-1beta, IL-6, IL-8, PGE2 along with its ability to override glucocorticoid activity in relation to TNF-alpha release from monocytes. However, our recent study has failed to reproduce findings on MIF as a factor with cytokine-inducing properties but it has confirmed that MIF is capable of inducing glucocorticoid-counter regulating activity and amplifying LPS-driven cytokine responses. The aim of this review is to analyse the plethora of data surrounding MIF not just as a cytokine, but also as a hormone-like molecule, enzyme with atypical properties and as a thioredoxin-like protein to address fundamental questions about MIF functionality.
巨噬细胞移动抑制因子（MIF）有着一段令人惊叹的历史，围绕其真正生物学功能不断有新发现和争议。它已被归类为一种强大的细胞因子，能够诱导肿瘤坏死因子（TNF）-α、白细胞介素-1β、白细胞介素-6、白细胞介素-8、前列腺素E2，同时它还具有在单核细胞释放TNF-α方面超越糖皮质激素活性的能力。然而，我们最近的研究未能重现MIF作为具有细胞因子诱导特性因子的相关发现，但证实了MIF能够诱导糖皮质激素反调节活性并放大脂多糖驱动的细胞因子反应。本综述的目的是分析围绕MIF的大量数据，不仅将其视为一种细胞因子，还将其视为一种类激素分子、具有非典型特性的酶以及一种硫氧还蛋白样蛋白，以解决有关MIF功能的基本问题。
