Table 2.

Interleukins associated with the immune evasion in breast cancer

Interleukins	Action on BC	Impact on tumor development	Impact on mechanism	References
IL-6	Promotion	Invasion↑ EMT	Take part in the activation of NF-κB signaling pathway by the activation of STAT3 and IL-6 receptor/GP130 complex, thus changing its phenotype to variants	103–105
IL-10	Promotion	Angiogenesis↑ Invasion↑	Activate CTL and NK cells, increase tumor infiltration, and inhibit metalloproteinase	114
	Inhibition	Growth↓ Metastasis↓	Induction of NK-mediated lysis of BC
IL-18	Promotion	Tumorigenesis↑ Distal metastasis↑	Activate CTL and NK cells and induce IFN-γ	109, 110
	Inhibition	Local impact
IL-19 and IL-20	Promotion	Growth↑ Proliferation↑ Progression↑	Synthesis of matrix metalloproteinase	111, 112
IL-23	Promotion	Inflammation↑	Modulate infiltration of CD8+ T cells and inflammation-related development of breast cancer microenvironment	113
IL-33	Tumor	Apoptosis of MDSC↓	Induce the autocrine production of GM-CSF Activate NF-κB and mitogen-activated protein kinase signaling	107

Notes: Different interleukins are listed in the table along with their influences on the immune evasion in breast cancer. ↑ means increase and ↓ means decrease.

Abbreviations: BC, breast cancer; IL, interleukin; NF-κB, nuclear factor-kappa B; STAT, signal transducer and activator of transcription; EMT, epithelial-to-mesenchymal transition; CTL, cytotoxic T lymphocyte; NK, natural killer; IFN-γ, interferon gamma; MDSC, myeloid-derived suppressor cell; GM-CSF, granulocyte–macrophage colony-stimulating factor.