Breast cancer (BC) is the most common type of cancer among females, and the number of deaths due to BC has increased over the past few decades. BC is primarily categorized based on the receptor status of BC cells as hormone receptor-positive (HR+), human epidermal growth factor receptor 2-positive (HER2+), and triple-negative BC (TNBC). These subtypes differ significantly in their treatment strategies, prognosis, immunogenic nature, and response to immunotherapy. TNBC is the most aggressive with a poor prognosis, but a subset of TNBCs that express programmed cell death ligand 1, have shown promising responses to immune checkpoint inhibitors. Across BC subtypes, distinct immune cell subsets remain active in the tumor immune microenvironment (TIME) that either inhibit or promote the growth of cancer. In isolation, it is challenging for cancer cells to thrive in presence of the body’s immune system, however with the aid of other cells in the TIME, they can work together to evade immune detection by suppressing antigen presentation, modulating immune recognition markers, and recruiting immune-suppressive cells. In this review, we provide an overview of the BC immune evasion mechanisms and discuss aspects of immune evasion in relation to tumor heterogeneity and cellular plasticity. We also highlight successful clinical trials targeting immune-evasion markers and discuss the challenges and potential future directions for solving these problems.

Breast cancer, Tumor heterogeneity, Tumor immune microenvironments, Immune evasion, Clinical trials