@article{bc92eff525e141dc98caf8bc524be89e,
title = "Effector lymphocyte-induced lymph node-like vasculature enables naive T-cell entry into tumours and enhanced anti-tumour immunity",
abstract = "The presence of lymph node (LN)-like vasculature in tumours, characterized by expression of peripheral node addressin and chemokine CCL21, is correlated with T-cell infiltration and positive prognosis in breast cancer and melanoma patients. However, mechanisms controlling the development of LN-like vasculature and how it might contribute to a beneficial outcome for cancer patients are unknown. Here we demonstrate that LN-like vasculature is present in murine models of melanoma and lung carcinoma. It enables infiltration by naive T cells that significantly delay tumour outgrowth after intratumoral activation. Development of this vasculature is controlled by a mechanism involving effector CD8 T cells and NK cells that secrete LTα3 and IFNγ. LN-like vasculature is also associated with organized aggregates of B lymphocytes and gp38+ fibroblasts, which resemble tertiary lymphoid organs that develop in models of chronic inflammation. These results establish LN-like vasculature as both a consequence of and key contributor to anti-tumour immunity.",
author = "Peske, {J. David} and Thompson, {Elizabeth D.} and Lelisa Gemta and Baylis, {Richard A.} and Fu, {Yang Xin} and Engelhard, {Victor H.}",
note = "Funding Information: We thank Holly Davis for animal husbandry, Dr Kara Cummings for laboratory support and the entire Engelhard laboratory for insightful discussions and advice. We thank Dr Kodi Ravichandran for advice in preparing the manuscript and he along with Dr Kenneth Tung and Dr Loren Erickson for use of equipment; the UVA Research Histology Core for tissue sectioning; Dr E. Podack (University of Miami) for LLC-OVA; Dr Robert Schreiber (Washington University St Louis) for IFNg-neutralizing antibody; and Dr Marcus Bosenberg (Yale) for paraffin-embedded tumours from BRAFV600E PTEN−/− mice and BRAFV600E PTEN−/− with an activating mutation in b-catenin27,34. This work was supported by the United States Public Health Service (USPHS) grants CA78400 and CA181794 (V.H.E.), CA044579 (University of Virginia Cancer Center), training grants GM007267 and AI7496 (E.D.T.), and GM007267, CA009109 and the Farrow Fellowship (J.D.P.). Publisher Copyright: {\textcopyright} 2015 Macmillan Publishers Limited. All rights reserved.",
year = "2015",
month = may,
day = "13",
doi = "10.1038/ncomms8114",
language = "English (US)",
volume = "6",
journal = "Nature communications",
issn = "2041-1723",
publisher = "Nature Publishing Group",
}