Journal
NATURE IMMUNOLOGY
Volume 16, Issue 1, Pages 75-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.3035
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Funding
- US National Institutes of Health [R0I DK074500, P01 AI045757, R21 CA182598, 5R01 AI039246, P01 HL085607, GM103441]
- American Cancer Society
- Claudia Adams Barr Program in Innovative Cancer Research
- Cancer Research Institute
- American Heart Association [SDG7410022]
- National Science Foundation
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In lymph nodes, fibroblastic reticular cells (FRCs) form a collagen-based reticular network that supports migratory dendritic cells (DCs) and T cells and transports lymph. A hallmark of FRCs is their propensity to contract collagen, yet this function is poorly understood. Here we demonstrate that podoplanin (PDPN) regulates actomyosin contractility in FRCs. Under resting conditions, when FRCs are unlikely to encounter mature DCs expressing the PDPN receptor CLEC-2, PDPN endowed FRCs with contractile function and exerted tension within the reticulum. Upon inflammation, CLEC-2 on mature DCs potently attenuated PDPN-mediated contractility, which resulted in FRC relaxation and reduced tissue stiffness. Disrupting PDPN function altered the homeostasis and spacing of FRCs and T cells, which resulted in an expanded reticular network and enhanced immunity.
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