IGF1R is highly expressed in the armored & cold tumors, and collagen mediates IGF1R at the transcriptional and post-translational levels to promote TNBC cell invasion and immune escape and to stabilize its own structure by interacting with the collagen receptor DDR1. The combination of IGF1R inhibition and PD-1 monoclonal antibody b enhances TNBC immunotherapeutic effects. In conclusion, this study finds a new target IGF1R based on the armored & cold features and provides new molecular insights to find good immunotherapeutic options for TNBC. Abstract In the previous study, patients with tumors based on collagen deposition and immunoreactivity are classified and identified the armored & cold subtype as the most treatment-refractory tumor type. Triple-negative breast cancer (TNBC) is the most lethal tumor type globally, making it critical to overcome the armored and cold tumor microenvironment (TME) for effective treatment of these patients. In this study, the transcriptomic collagen activity and immune profiles of cancer patients treated with immune checkpoint blockade (ICB) are analyzed, and found that intratumoral collagen is associated with an unfavorable immunotherapeutic response and T cell exhaustion. Additionally, collagen is shown to regulate IGF1R expression at both transcriptional and post-translational levels via SOX4 and DDR1, respectively. It is also found that IGF1R promotes tumor cell migration and invasion, as well as T cell exhaustion, with these effects mediated through collagen. Moreover, in vivo inhibition of IGF1R reversed the armored & cold TME, thereby enhancing anti-PD-1 therapy. In conclusion, this study identified IGF1R as a novel therapeutic target for the immuno-collagenic subtype, and combining IGF1R inhibition with anti-PD-1 therapy provides a promising foundation for a novel combination immunotherapy regimen for TNBC.