Is MIF a central messenger in colitis?

Abstract

Dissection of interactions between gut mucosa and commensal organisms has demonstrated significant roles for T cells. In the pathological inflammation seen in colitis, activated T cells interacting with products from these gut flora produce Th1-type cytokines. Pharmacological treatment with anti-tumour necrosis factor (TNF)-α or interleukin (IL)-10 give some benefit in colitis, a disease whose clinical management remains a challenge. However, several lines of evidence suggest that gut Tcells might be regulated by macrophages in colitis. The mediators involved in these communications could offer another point for therapeutic intervention, particularly in those patients who do not respond to T-cell-directed therapies. Macrophage migration inhibitory factor (MIF) is one such cytokine. It reduces movement of macrophages invitro, and is associated with macrophage–T-cell interactions in delayed-type hypersensitivity responses.