¹Centre for Molecular Medicine, University of Manchester, Manchester, UK

Correspondence: Dr A Kudrin, Department of Rheumatology, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0QQ, UK. E-mail: alexkudrin@aol.com

Received 11 September 2007; Revised 8 October 2007; Accepted 9 October 2007; Published online 27 November 2007.

Abstract

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)-, IL-1, IL-6, IL-8, PGE2 along with its ability to override glucocorticoid activity in relation to TNF- 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.