Macrophage migration inhibitory factor and glucocorticoid sensitivity
Review published in Rheumatology (Oxford, England) (2006)
Abstract
Glucocorticoids (GCs) are widely used in the treatment of inflammatory diseases including rheumatoid arthritis (RA). Treatment with GC is associated with significant dose-dependent side-effects. The pro-inflammatory cytokine macrophage migration inhibitory factor (MIF) has emerged in recent years as a candidate factor which could regulate GC sensitivity. MIF is induced by GC, and is able to override anti-inflammatory actions of GCs. In this review, we summarize the pro-inflammatory actions of MIF with respect to RA, describe the interactions between MIF and GC and examine new evidence, which identifies MIF as a specific target for steroid sparing.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Summary
Glucocorticoids (GCs) are widely used in the treatment of inflammatory diseases including rheumatoid arthritis (RA).
Why This Matters for Hirudotherapy
This review examines macrophage migration inhibitory factor (MIF) as a regulator of glucocorticoid sensitivity in inflammatory diseases including rheumatoid arthritis, describing how MIF can override the anti-inflammatory actions of glucocorticoids and identifying MIF as a target for steroid-sparing therapies. There is no defensible leech or hirudotherapy link in this abstract; it contains no mention of thrombin, coagulation, leeches, or any leech-derived compound. The subject matter concerns cytokine biology and steroid pharmacology in autoimmunity, which falls entirely outside ASH's domain of hirudotherapy and the leech secretome. This article appears to have no relevance to ASH's research library.
Citation
Macrophage migration inhibitory factor and glucocorticoid sensitivity
Aeberli D et al. · Rheumatology (Oxford, England), 2006
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