Folate receptor‐β constitutes a marker for human proinflammatory monocytes. Issue 4 (11th July 2014)

• Record Type: Journal Article
• Authors: Shen, Jiayin; Hilgenbrink, Andrew R.; Xia, Wei; Feng, Yang; Dimitrov, Dimiter S.; Lockwood, Michael B.; Amato, Robert J.; Low, Philip S.
• Is Part Of: Journal of leukocyte biology. Volume 96:Issue 4(2014)
• Page Start: 563
• Page End: 570
• Publication Date: 2014-07-11
• Subjects: inflammatory subset -- folate targeting -- immunotherapy -- inflammation; Leucocytes -- Periodicals; Reticulo-endothelial system -- Periodicals; 571.96
• DOI: 10.1189/jlb.2AB0713-372R
• Languages: English
• ISSNs: 0741-5400

Abstract

Abstract : Folate receptor‐β mediated targeting of inflammatory monocytes in inflammation. Abstract : Activated macrophages are commonly involved in the pathogenesis of inflammatory and autoimmune diseases and have been frequently reported to overexpress FR‐β. Although FR‐targeted therapies aimed at eliminating activated macrophages have shown promise for treating inflammatory diseases, little work has been performed to evaluate whether other hematopoietic cells might also express FR‐β. Analysis of peripheral blood cells with a mAb to human FR‐β reveals that only monocytes express FR‐β. Molecular characterization of these circulating monocytes further demonstrates that solely the classic/proinflammatory subset (CD14 high CD16 − ) expresses the FR and that only CD14 high CD16 − FR‐β + monocytes also display the ability to bind folate‐linked molecules. Confirmation that this subset of monocytes indeed constitutes the proinflammatory subpopulation was obtained by demonstrating coexpression of FR‐β with other proinflammatory markers, including CCR2 and HLA‐DR. Synovial monocytes from the joints of patients with RA were also shown to express FR‐β. As inhibition of the chemotaxis of proinflammatory monocytes into sites of inflammation has been explored frequently as a means of controlling autoimmune diseases, demonstration that FR‐β is uniquely expressed on this proinflammatory subpopulation offers a new strategy to suppress migration of inflammatory monocytes into sites of inflammation.