Placental growth factor regulates the generation of T(H)17 cells to link angiogenesis with autoimmunity

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Helper T cells actively communicate with adjacent cells by secreting soluble mediators, yet crosstalk between helper T cells and endothelial cells remains poorly understood. Here we found that placental growth factor (PIGF), a homolog of the vascular endothelial growth factor that enhances an angiogenic switch in disease, was selectively secreted by the T(H)17 subset of helper T cells and promoted angiogenesis. Interestingly, the 'angio-lymphokine' PIGF, in turn, specifically induced the differentiation of pathogenic T(H)17 cells by activating the transcription factor STAT3 via binding to its receptors and replaced the activity of interleukin-6 in the production of interleukin-17, whereas it suppressed the generation of regulatory T cells. Moreover, T cell-derived PIGF was required for the progression of autoimmune diseases associated with T(H)17 differentiation, including experimental autoimmune encephalomyelitis and collagen-induced arthritis, in mice. Collectively, our findings provide insights into the PIGF-dictated links among angiogenesis, T(H)17 cell development and autoimmunity.
Publisher
NATURE PUBLISHING GROUP
Issue Date
2019-10
Language
English
Article Type
Article
Citation

NATURE IMMUNOLOGY, v.20, no.10, pp.1348 - +

ISSN
1529-2908
DOI
10.1038/s41590-019-0456-4
URI
http://hdl.handle.net/10203/267839
Appears in Collection
MSE-Journal Papers(저널논문)
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