STAT of the union : dynamics of distinct tumor-associated macrophage subsets governed by STAT1

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Abstract

The tumor stroma has long been ignored as therapeutic target, but it has become clear that several stromal cell types play a nonredundant role during tumor progression. In particular, macrophages possess the capacity to stimulate tumor growth and metastasis via multiple mechanisms. In this issue of the European Journal of Immunology, a study by Tymoszuk et al. Eur. J. Immunol. 2014. 44: 2247-2262 demonstrates that both monocyte recruitment and local macrophage proliferation determines the tumor-associated macrophage (TAM) pool size in HER2/Neu-driven mammary carcinomas. These tumors contain two main TAM subsets--MHC class II (MHC-II)loF4/80hi and MHC-IIhiF4/80lo--similar to what was observed in other tumor models. Interestingly, only the MHC-IIloF4/80hi subset is largely absent in a STAT1-deficient background. STAT1 induces the expression of CSF-1, which in turn drives TAM proliferation and possibly also the M2 gene signature of MHC-IIloF4/80hi TAM. Conversely, STAT1 deficiency upregulates M2 gene expression in MHC-IIhiF4/80lo TAM, demonstrating that both TAM subsets are differentially regulated, probably as a consequence of their distinct intratumoral localization. In this Commentary, we place these findings in the context of current knowledge and propose new avenues for future research.
Original languageEnglish
Pages (from-to)2238-2242
Number of pages5
JournalEur. J. Immunol.
Volume44
Publication statusPublished - 1 Aug 2014

Keywords

  • CSF-1
  • Ontogeny
  • Stat1
  • Tumor-associated macrophages

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