Breast cancer remains the most frequently diagnosed malignancy among women worldwide and is a leading cause of cancer-related mortality. A growing body of research indicates that immunological dysregulation and chronic inflammation are important factors in the development, spread, invasion, and metastasis of breast cancer. In the tumour microenvironment, interleukins (ILs), a broad class of cytokines involved in inflammatory responses and immune control, have become important mediators. The biological roles of key interleukins and their connection to the pathophysiology of breast cancer are outlined in this article. Through various signalling pathways, a number of interleukins, such as IL-1, IL-6, IL-8, IL-10, IL-11, IL-13, IL-17, IL-19, IL-21, IL-23, IL-32, and IL-33, contribute to tumour growth, angiogenesis, immune evasion, epithelial–mesenchymal transition, and metastatic dissemination. Aggressive tumour characteristics, a poor prognosis, treatment resistance, and lower survival rates have all been linked to elevated expression of these cytokines. On the other hand, some interleukins have anti-tumor properties through boosting immune surveillance and encouraging cytotoxic reactions against cancerous cells. Genetic variables such BRCA1, BRCA2, HER2, TP53, and vitamin D receptor polymorphisms affect breast cancer susceptibility and disease development in addition to cytokine-mediated processes. Gaining an understanding of the intricate relationships that exist between interleukins, tumour cells, and the immunological milieu may help uncover new biomarkers for diagnosis, prognosis, and targeted treatment. Future research on interleukin-based treatment approaches may help enhance clinical results and provide patients with breast cancer with more individualised care.