In a transgenic mouse model of AD, the activation of T and B lymphocytes was increased [88], and these lymphocytes could produce high levels of IL-2, granulocyte macrophage-colony stimulating factor (GM-CSF), tumor necrosis factor-alpha (TNF-α), and IL-17, which pointed to the Th17 polarization [88]. The gene discussed is IL17A; the disease is Alzheimer disease.