Editorial: Sticking it to fibrocytes with serum amyloid P

Abstract

Fibrocytes are a bone marrow-derived mesenchymal population whose existence was first proposed over 150 years ago following the detailed microscopic observations of James Paget [1]. Whereas bloodborne connective tissue cell precursors are also described in the writings of Cohnheim, Metchnikov, Fischer, and Maximow [1], it was not until 1994 that the term “fibrocyte” was coined to describe this unique population of cells possessing the tissue-remodeling properties of fibroblasts and the proinflammatory properties of monocytes [2, 3]. Accumulating data gleaned from animal modeling and human studies suggest that circulating and/or local fibrocytes contribute to a broad range of chronic inflammatory conditions, including those affecting the lung, liver, autoimmune disease, skin, and even normal aging [3]. Fibrocyte differentiation is suppressed by serum amyloid P (SAP) [4], a short pentraxin protein that is produced by the liver as an acute-phase reactant. Interestingly, whereas the in vivo activitiy of SAP on human fibrocyte biology appears to involve certain Fc gamma receptors (FcγRs) and aggregated IgG [5], the precise mechanism of the inhibitory effects of SAP on the monocyte-to-fibrocyte transition remains unclear.