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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.

Original publication

DOI

10.1038/sj.icb.7100133

Type

Journal article

Journal

Immunol Cell Biol

Publication Date

03/2008

Volume

86

Pages

232 - 238

Keywords

Acetaminophen, Animals, Cell Movement, Disease Susceptibility, Feedback, Physiological, Glucocorticoids, Humans, Intramolecular Oxidoreductases, Macrophage Migration-Inhibitory Factors, Oxidation-Reduction, Polymorphism, Genetic, Reducing Agents, T-Lymphocytes