Cytokines, inflammation and breast cancer

Abstract

Infection, cancer, or inflammation triggers the production of immunological mediators termed cytokines. Some cytokines clearly promote inflammation and are called pro-inflammatory cytokines, whereas other cytokines suppress the activity of pro-inflammatory cytokines and are called anti-inflammatory cytokines. For example, IL-4, IL-10, and IL-13 are potent activators of B lymphocytes. However, IL-4, IL-10, and IL-13 are also potent anti-inflammatory agents. They are anti-inflammatory cytokines by virtue of their ability to suppress genes for pro-inflammatory cytokines such as IL-1, TNF, and the chemokines. IL-1 and TNF are inducers of endothelial adhesion molecules, which are essential for the adhesion of leukocytes to the endothelial surface prior to emigration into the tissues. Taken together, pro-inflammatory cytokine mediated inflammation is a cascade of gene products usually not produced in healthy persons. Anti-inflammatory cytokines block this process or at least suppress the intensity of the cascade. Cytokines such as IL-4, IL-10, IL-13, and transforming growth factor (TGF-β) suppress the production of IL-1, TNF, chemokines such as IL-8, and vascular adhesion molecules. Therefore, a “balance†between the effects of pro-inflammatory and anti-inflammatory cytokines is thought to determine the outcome of disease, whether in the short term or long term. This article reviews the functions of the cytokines in relation to breast cancer.