Verdeil G Lawrence T Schmitt-Verhulst AM Auphan-Anezin N 2019 Oncogene-induced STAT3-activation is central to tumor progression by promoting cancer cell expression of pro-angiogenic and immunosuppressive factors. STAT3 is also activated in infiltrating immune cells including tumor-associated macrophages (TAM) amplifying immune suppression. Consequently, STAT3 is considered as a target for cancer therapy. However, its interplay with other STAT-family members or transcription factors such as NF-κB has to be considered in light of their concerted regulation of immune-related genes. Here, we discuss new attempts at re-educating immune suppressive tumor-associated macrophages towards a CD8 T cell supporting profile, with an emphasis on the role of STAT transcription factors on TAM functional programs. Recent clinical trials using JAK/STAT inhibitors highlighted the negative effects of these molecules on the maintenance and function of effector/memory T cells. Concerted regulation of STAT3 and STAT5 activation in CD8 T effector and memory cells has been shown to impact their tumor-specific responses including intra-tumor accumulation, long-term survival, cytotoxic activity and resistance toward tumor-derived immune suppression. Interestingly, as an escape mechanism, melanoma cells were reported to impede STAT5 nuclear translocation in both CD8 T cells and NK cells. Ours and others results will be discussed in the perspective of new developments in engineered T cell-based adoptive therapies to treat cancer patients. application/pdf https://sonar.ch/global/documents/186365 eng info:eu-repo/semantics/altIdentifier/doi/10.3390/cancers11121832 info:eu-repo/semantics/altIdentifier/pmid/31766350 info:eu-repo/semantics/openAccess Cancers. - 2019 STAT transcription factors adoptive T cell therapy immune suppression inflammation tumor-associated macrophages Targeting STAT3 and STAT5 in Tumor-Associated Immune Cells to Improve Immunotherapy. http://purl.org/coar/resource_type/c_6501