SCS macrophages suppress melanoma by restricting tumor-derived vesicle–B cell interactions | Zendy

Ferdinando Pucci | Zendy; Christopher Garris | Zendy; Charles PinKuang Lai | Zendy; Andita Newton | Zendy; Christina Pfirschke | Zendy; Camilla Engblom | Zendy; David Álvarez | Zendy; Melissa M. Sprachman | Zendy; Charles L. Evavold | Zendy; Angela M. Magnuson | Zendy; Ulrich H. von Andrian | Zendy; Katharina Glatz | Zendy; Xandra O. Breakefield | Zendy; Thorsten R. Mempel | Zendy; Ralph Weissleder | Zendy; Mikaël J. Pittet | Zendy

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SCS macrophages suppress melanoma by restricting tumor-derived vesicle–B cell interactions

Author(s) -

Ferdinando Pucci,

Christopher Garris,

Charles PinKuang Lai,

Andita Newton,

Christina Pfirschke,

Camilla Engblom,

David Álvarez,

Melissa M. Sprachman,

Charles L. Evavold,

Angela M. Magnuson,

Ulrich H. von Andrian,

Katharina Glatz,

Xandra O. Breakefield,

Thorsten R. Mempel,

Ralph Weissleder,

Mikaël J. Pittet

Publication year - 2016

Publication title -

science

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 12.556

H-Index - 1186

eISSN - 1095-9203

pISSN - 0036-8075

DOI - 10.1126/science.aaf1328

Subject(s) - lymph , immune system , melanoma , extracellular vesicles , cancer research , population , tumor cells , tumor microenvironment , microvesicles , biology , immunology , microbiology and biotechnology , medicine , pathology , genetics , microrna , environmental health , gene

Tumor-derived extracellular vesicles (tEVs) are important signals in tumor-host cell communication, yet it remains unclear how endogenously produced tEVs affect the host in different areas of the body. We combined imaging and genetic analysis to track melanoma-derived vesicles at organismal, cellular, and molecular scales to show that endogenous tEVs efficiently disseminate via lymphatics and preferentially bind subcapsular sinus (SCS) CD169(+) macrophages in tumor-draining lymph nodes (tdLNs) in mice and humans. The CD169(+) macrophage layer physically blocks tEV dissemination but is undermined during tumor progression and by therapeutic agents. A disrupted SCS macrophage barrier enables tEVs to enter the lymph node cortex, interact with B cells, and foster tumor-promoting humoral immunity. Thus, CD169(+) macrophages may act as tumor suppressors by containing tEV spread and ensuing cancer-enhancing immunity.

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