Abstract
Tumors require a constant influx of myelomonocytic cells to support the
angiogenesis and stroma remodeling needed for their growth. This is mediated by
tumor-derived factors, which cause sustained myelopoiesis and the accumulation
and functional differentiation of myelomonocytic cells, most of which are
macrophages, at the tumor site. An important side effect of the accumulation and
functional differentiation of these cells is that they can induce lymphocyte
dysfunction. A complete understanding of the complex interplay between
neoplastic and myelomonocytic cells might offer novel targets for therapeutic
intervention aimed at depriving tumor cells of important growth support and
enhancing the antitumor immune response.
Authors
Antonio Sica, Vincenzo Bronte
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