Crosstalk between tumor-infiltrating immune cells and cancer-associated Fibroblasts in tumor growth and immunosuppression of breast cancer
Signals from the tumor microenvironment (TME) have a profound influence on the maintenance and progression of cancers. Chronic inflammation and the infiltration of immune cells in breast cancer (BC) have been strongly associated with early carcinogenic events and a switch to a more immunosuppressive response. Cancer-associated fibroblasts (CAFs) are the most abundant stromal component and can modulate tumor progression according to their secretomes. The immune cells including tumor-infiltrating lymphocytes (TILs) (cytotoxic T cells (CTLs), regulatory T cells (Tregs), and helper T cell (Th)), monocyteinfiltrating cells (MICs), myeloid-derived suppressor cells (MDSCs), mast cells (MCs), and natural killer cells (NKs) play an important part in the immunological balance, fluctuating TME between protumoral and antitumoral responses. In this review article, we have summarized the impact of these immunological players together with CAF secreted substances in driving BC progression. We explain the crosstalk of CAFs and tumor-infiltrating immune cells suppressing antitumor response in BC, proposing these cellular entities as predictive markers of poor prognosis. CAF-tumor-infiltrating immune cell interaction is suggested as an alternative therapeutic strategy to regulate the immunosuppressive microenvironment in BC. ; Comision Nacional de Investigacion Cientifica y Tecnologica (CONICYT) CONICYT FONDECYT 11190990 3190931 National Commission for Scientific and Technological Research REDES Chile 180134 Thailand Science Research and Innovation, National Research Council of Thailand (NRCT), Ministry of Higher Education, Science, Research and Innovation Thailand RSA6280091 Faculty of Medicine Siriraj Hospital, Mahidol University R016033015 ANID (National Research and Development Agency from the Chilean Government; Program of International Cooperation to Support for the Formation of International Networks between Research Centers) 180134 ; Versión publicada - versión final del editor