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Journal of Immunology Research
Volume 2016, Article ID 6031486, 16 pages
Research Article

Monocyte Differentiation towards Protumor Activity Does Not Correlate with M1 or M2 Phenotypes

1Unidad de Investigación en Virología y Cáncer, Hospital Infantil de México Federico Gómez, Dr. Márquez 162, Colonia Doctores, 06720 Ciudad de México, DF, Mexico
2Programa de Doctorado en Ciencias Biomédicas, Universidad Nacional Autónoma de México (UNAM), 04510 Ciudad de México, DF, Mexico
3UIM en Inmunología, Hospital de Pediatría, CMN Siglo XXI, IMSS, 06720 Ciudad de México, DF, Mexico
4UIM en Inmunoquímica, Hospital de Especialidades, CMN Siglo XXI, IMSS, 06720 Ciudad de México, DF, Mexico

Received 11 March 2016; Accepted 4 May 2016

Academic Editor: Oscar Bottasso

Copyright © 2016 G. Karina Chimal-Ramírez et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Macrophages facilitate breast cancer progression. Macrophages were initially classified as M1 or M2 based on their distinct metabolic programs and then expanded to include antitumoral (M1) and protumoral (M2) activities. However, it is still uncertain what markers define the pro- and antitumoral phenotypes and what conditions lead to their formation. In this study, monocytic cell lines and primary monocytes were subjected to commonly reported protocols of M1/M2 polarization and conditions known to engage monocytes into protumoral functions. The results showed that only IDO enzyme and CD86 M1 markers were upregulated correlating with M1 polarization. TNF-α, CCR7, IL-10, arginase I, CD36, and CD163 were expressed indistinguishably from M1 or M2 polarization. Similarly, protumoral engaging resulted in upregulation of both M1 and M2 markers, with conditioned media from the most aggressive breast cancer cell line promoting the greatest changes. In spite of the mixed phenotype, M1-polarized macrophages exhibited the highest expression/secretion of inflammatory mediators, many of which have previously been associated with breast cancer aggressiveness. These data argue that although the existence of protumoral macrophages is unquestionable, their associated phenotypes and the precise conditions driving their formation are still unclear, and those conditions may need both M1 and M2 stimuli.