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Silence STAT3 in the procancer niche… and activate CD8+ T cells to kill premetastatic myeloid intruders.

Authors
  • Auphan-Anezin, Nathalie
  • Schmitt-Verhulst, Anne-Marie
Type
Published Article
Journal
European Journal of Immunology
Publisher
Wiley
Publication Date
Jan 01, 2015
Volume
45
Issue
1
Pages
44–48
Identifiers
DOI: 10.1002/eji.201445300
PMID: 25471823
Source
Medline
Keywords
License
Unknown

Abstract

Several recent studies have implicated myeloid cells in providing a microenvironment that promotes tumor cell survival and metastasis, therefore preparing a "premetastatic niche" for cancer progression. In this issue of the European Journal of Immunology, Zhang et al. [Eur. J. Immunol. 2015. 45: 71-81] address the regulation of immune cells in premetastatic lymph nodes in experimental mouse models. The authors show that signal transducer and activator of transcription 3 (STAT3) ablation in murine myeloid cells, which renders the premetastatic niche less receptive to metastasis by B16 melanoma cells, also leads to local activation in the niche of CD8(+) T cells with increased expression of IFN-γ and granzyme B. Data further suggest that STAT3 activation in the myeloid population leads to poor tumor antigen presenting capacity as well as resistance to CD8(+) T-cell killing. Based on these studies in mice and observations in human cancer patients, the authors propose treatments designed to regulate STAT3 activation, which are correlated with increased cytolytic activity of CD8(+) T cells in mouse models.

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