This chapter provides an integrated overview of how innate and adaptive immunity jointly protect the host from pathogens and malignant transformation. Innate immunity delivers rapid, nonspecific defense through physical barriers, phagocytes, NK cells, pattern-recognition receptors, and inflammatory mediators. Adaptive immunity, mediated by somatically recombined B cell receptors (BCRs) and T cell receptors (TCRs), enables highly specific antigen recognition, immunological memory, and cytotoxic elimination of infected or transformed cells. A central theme is the balance between immune protection and immune-mediated damage, reflected in phenomena such as autoimmunity, allergy, and transplant rejection. We describe inflammation as an evolutionarily conserved response that can become chronic when stimuli persist, promoting metabolic disease, tissue dysfunction, and cancer. Age-related immune alterations, immunosenescence, inflammaging, reduced TCR diversity, impaired dendritic cell function, and clonal hematopoiesis significantly weaken cancer immunosurveillance. Cancer immunity is governed by the cancer-immune cycle, neoantigen presentation, and immune editing, but tumors evolve multiple evasion strategies, including MHC downregulation, PD-L1 upregulation, metabolic suppression, and epigenetic plasticity. Modern immunotherapies, checkpoint inhibitors, monoclonal antibodies, neoantigen vaccines, and CAR-T and CAR-NK cell therapies seek to restore and amplify antitumor immunity. Their efficacy is influenced by tumor mutational burden, immune contexture, aging, metabolic states, stress biology, and lifestyle factors such as exercise and obesity. Collectively, we highlight immunity as both a barrier to cancer and a therapeutic tool.