| First Author | Fridlender ZG | Year | 2009 |
| Journal | Cancer Cell | Volume | 16 |
| Issue | 3 | Pages | 183-94 |
| PubMed ID | 19732719 | Mgi Jnum | J:152379 |
| Mgi Id | MGI:4358626 | Doi | 10.1016/j.ccr.2009.06.017 |
| Citation | Fridlender ZG, et al. (2009) Polarization of tumor-associated neutrophil phenotype by TGF-beta: 'N1' versus 'N2' TAN. Cancer Cell 16(3):183-94 |
| abstractText | TGF-beta blockade significantly slows tumor growth through many mechanisms, including activation of CD8(+) T cells and macrophages. Here, we show that TGF-beta blockade also increases neutrophil-attracting chemokines, resulting in an influx of CD11b(+)/Ly6G(+) tumor-associated neutrophils (TANs) that are hypersegmented, more cytotoxic to tumor cells, and express higher levels of proinflammatory cytokines. Accordingly, following TGF-beta blockade, depletion of these neutrophils significantly blunts antitumor effects of treatment and reduces CD8(+) T cell activation. In contrast, in control tumors, neutrophil depletion decreases tumor growth and results in more activated CD8(+) T cells intratumorally. Together, these data suggest that TGF-beta within the tumor microenvironment induces a population of TAN with a protumor phenotype. TGF-beta blockade results in the recruitment and activation of TANs with an antitumor phenotype. |
