Richard Bucala

TL;DR: The results suggest that CD45+/Col1+ cells may be directly involved, in part through CCL2/CCR2 signaling, in the fibrotic process under diabetic conditions.

Abstract: This chapter provides an overview of macrophage migration inhibitory factor (MIF), which is a critical pro-inflammatory mediator that has been found to play an important role in diverse conditions characterized both by inflammation and cellular proliferation. MIF has a number of unique structural, genetic, and functional properties that distinguish it from other cytokines. These properties include unique tertiary structure, catalytic activity, a non-conventional secretory pathway, widespread expression and secretion from endocrine as well as immune cells, and its action as an endogenous counter-regulator of the anti-inflammatory and immunosuppressive properties of steroids. Also, MIF is unique in being a “pro-inflammatory” mediator that is induced in cells by glucocorticoids. Consistent with the wide range of activities of MIF, it has been found to be involved in the pathogenesis of many conditions. Important areas of future investigation includes in identifying the nature, and regulation of the MIF receptor, understanding the regulation of MIF at the genetic level, and designing clinically effective means of inhibiting its activity.

TL;DR: Data indicate that MIF deficiency is associated with a compensatory amplification of γδ17 cell responses, with implications for innate immunity and IL‐17‐mediated pathology in situations such as gram‐positive toxic shock or Mycobacterium infection.

TL;DR: This study suggests an association between a common genetic polymorphism of an endogenous innate immune gene, MIF, with reduced DLCO, an important measurement of COPD severity.

TL;DR: Pulmonary arterial hypertension (PAH) is a severe complication of systemic lupus erythematosus (SLE), with unclear etiopathogenesis, and MIF may serve as a biomarker and a therapeutic target of SLE-associated PAH.