Journal
CURRENT RHEUMATOLOGY REPORTS
Volume 21, Issue 7, Pages -Publisher
SPRINGER
DOI: 10.1007/s11926-019-0831-z
Keywords
Systemic sclerosis; Scleroderma; Monocytes; Macrophages; Innate immunity; Fibrosis
Categories
Funding
- National Institute of Arthritis and Musculoskeletal and Skin Diseases [R56-AR0639835, R03-AR068097]
- Scleroderma Foundation
- National Institutes of Health p50 Specialized Center Grant [3P50AR060780 - 07W1]
- John H. Copenhaver, Jr. and William H. Thomas, MD 1952 Junior Fellowship from Dartmouth Graduate Studies
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Purpose of ReviewMacrophages play key roles in tissue homeostasis and immune surveillance, mobilizing immune activation in response to microbial invasion and promoting wound healing to repair damaged tissue. However, failure to resolve macrophage activation can lead to chronic inflammation and fibrosis, and ultimately to pathology. Activated macrophages have been implicated in the pathogenesis of systemic sclerosis (SSc), although the triggers that induce immune activation in SSc and the signaling pathways that underlie aberrant macrophage activation remain unknown.Recent FindingsMacrophages are implicated in fibrotic activation in SSc. Targeted therapeutic interventions directed against SSc macrophages may ameliorate inflammation and fibrosis.SummaryWhile current studies have begun to elucidate the role of macrophages in disease initiation and progression, further work is needed to address macrophage subset heterogeneity within and among SSc end-target tissues to determine the disparate functions mediated by these subsets and to identify additional targets for therapeutic intervention.
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