Tumour hypoxia promotes tolerance and angiogenesis via CCL28 and Treg cells View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2011-07-13

AUTHORS

Andrea Facciabene, Xiaohui Peng, Ian S. Hagemann, Klara Balint, Andrea Barchetti, Li-Ping Wang, Phyllis A. Gimotty, C. Blake Gilks, Priti Lal, Lin Zhang, George Coukos

ABSTRACT

Although immune mechanisms can suppress tumour growth, tumours establish potent, overlapping mechanisms that mediate immune evasion. Emerging evidence suggests a link between angiogenesis and the tolerance of tumours to immune mechanisms. Hypoxia, a condition that is known to drive angiogenesis in tumours, results in the release of damage-associated pattern molecules, which can trigger the rejection of tumours by the immune system. Thus, the counter-activation of tolerance mechanisms at the site of tumour hypoxia would be a crucial condition for maintaining the immunological escape of tumours. However, a direct link between tumour hypoxia and tolerance through the recruitment of regulatory cells has not been established. We proposed that tumour hypoxia induces the expression of chemotactic factors that promote tolerance. Here we show that tumour hypoxia promotes the recruitment of regulatory T (T(reg)) cells through induction of expression of the chemokine CC-chemokine ligand 28 (CCL28), which, in turn, promotes tumour tolerance and angiogenesis. Thus, peripheral immune tolerance and angiogenesis programs are closely connected and cooperate to sustain tumour growth. More... »

PAGES

226

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nature10169

    DOI

    http://dx.doi.org/10.1038/nature10169

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1025904798

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/21753853


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