Tumor-associated fibrosis is characterized by unchecked pro-fibrotic and pro-inflammatory signaling. The components of fibrosis including significant numbers of cancer-associated fibroblasts, dense collagen deposition, and extracellular matrix stiffness, are well appreciated regulators of tumor progression but may also be critical regulators of immune surveillance. While this suggests that the efficacy of immunotherapy may be limited in highly fibrotic cancers like pancreas, it also suggests a therapeutic opportunity to target fibrosis in these tumor types to reawaken anti-tumor immunity. This review discusses the mechanisms by which fibrosis might subvert tumor immunity and how to overcome these mechanisms.

Author Info: (1) Department of Medicine, Washington University School of Medicine, 660 South Euclid Ave., Box 8069, St. Louis, MO, 63110, USA. ICCE Institute, Washington University School of Me

Author Info: (1) Department of Medicine, Washington University School of Medicine, 660 South Euclid Ave., Box 8069, St. Louis, MO, 63110, USA. ICCE Institute, Washington University School of Medicine, St. Louis, MO, 63110, USA. (2) Department of Medicine, Washington University School of Medicine, 660 South Euclid Ave., Box 8069, St. Louis, MO, 63110, USA. ICCE Institute, Washington University School of Medicine, St. Louis, MO, 63110, USA. (3) Department of Medicine, Washington University School of Medicine, 660 South Euclid Ave., Box 8069, St. Louis, MO, 63110, USA. ddenardo@dom.wustl.edu. Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, 63110, USA. ddenardo@dom.wustl.edu. ICCE Institute, Washington University School of Medicine, St. Louis, MO, 63110, USA. ddenardo@dom.wustl.edu. Siteman Cancer Center, Washington University School of Medicine, St. Louis, MO, 63110, USA. ddenardo@dom.wustl.edu.