Update on macrophages and innate immunity in scleroderma.
OBJECTIVE
In this review of the literature from 2014 through mid-2015, we examine new data that shed light on how macrophages and other innate immune cells and signals contribute to inflammation, vascular dysfunction, and fibrosis in scleroderma.


RESULTS
Recent human studies have focused on changes early in scleroderma, and linked macrophages to inflammation in skin and progression of lung disease. Plasmacytoid dendritic cells have been implicated in vascular dysfunction. In mice, several factors have been identified that influence macrophage activation and experimental fibrosis. However, emerging data also suggest that myeloid cells can have differential effects in fibrosis. Sustained signaling through different toll-like receptors can lead to inflammation or fibrosis, and these signals can influence both immune and nonimmune cells.


CONCLUSIONS
There are many types of innate immune cells that can potentially contribute to scleroderma and will be worth exploring in detail. Experimentally dissecting the roles of macrophages based on ontogeny and activation state, and the innate signaling pathways in the tissue microenvironment, may also lead to better understanding of scleroderma pathogenesis.
aWeill Cornell/Rockefeller/Sloan-Kettering Tri-Institutional MD-PhD Program bImmunology and Microbial Pathogenesis Program, Weill Cornell Graduate School of Medical Sciences cAutoimmunity and Inflammation Program dAutoimmunity and Inflammation Program and Department of Pediatric Rheumatology, Hospital for Special Surgery eDepartment of Microbiology and Immunology, Weill Cornell Medical College, New York, USA.
Jennifer J
JJ
Chia
Theresa T
TT
Lu
D000818:Animals; D003713:Dendritic Cells / Q000276:immunology; D005355:Fibrosis / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation / Q000276:immunology; D008264:Macrophages / Q000276:immunology*; D051379:Mice; D012595:Scleroderma, Systemic / Q000276:immunology*