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Updated: May 27, 2026

Isolation of Human Lymphatic Endothelial Cells by Multi-parameter Fluorescence-activated Cell Sorting
Published on: May 1, 2015
Impaired lymphatic contraction associated with immunosuppression.
Shan Liao1, Gang Cheng, David A Conner
1EL Steele Laboratory, Department of Radiation Oncology, Harvard Medical School and Massachusetts General Hospital, Boston, MA 02114, USA.
Nitric oxide synthase (NOS) enzymes regulate lymphatic vessel function. Endothelial NOS (eNOS) drives contractions, while inducible NOS (iNOS) from inflammatory cells inhibits them, impacting immune responses.
Area of Science:
- Immunology
- Vascular Biology
- Physiology
Background:
- Collecting lymphatic vessels are crucial for immune cell transport to lymph nodes.
- Regulation of lymphatic vessel function and lymph transport remains poorly understood.
- Understanding lymphatic vessel contraction is key to immune response modulation.
Purpose of the Study:
- To investigate the molecular mechanisms regulating lymphatic vessel contraction.
- To develop a novel method for real-time imaging of lymphatic vessel function.
- To elucidate the role of nitric oxide synthases in lymphatic contractility.
Main Methods:
- Developed a unique mouse model for intravital imaging of autonomous lymphatic vessel contraction.
- Utilized this model to assess the impact of endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) on lymphatic function.
- Investigated the effects of inflammatory cell-derived iNOS on lymphatic contraction in an immune-induced multiple sclerosis model.
Main Results:
- Endothelial nitric oxide synthase (eNOS) is essential for normal lymphatic vessel contraction.
- Inflammatory CD11b(+)Gr-1(+) cells expressing iNOS significantly inhibit lymphatic contraction.
- Inhibition of lymphatic contraction by iNOS-expressing cells correlates with reduced antigen response in an experimental autoimmune encephalomyelitis model.
Conclusions:
- Nitric oxide synthases play a dual role in regulating lymphatic vessel function.
- CD11b(+)Gr-1(+) cell-mediated suppression of lymphatic function may protect against autoreactive responses during inflammation.
- This research provides a novel platform for studying lymphatic disorders and immune regulation.
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