Human monocytes were shown to trigger T-helper responses during infection and in autoimmune diseases.49,50 Nonclassical monocytes produce higher TNF after stimulation and expand under infectious or inflammatory conditions.18 Nonclassical monocytes in ITP promote Th1 development, which in turn negatively regulates interleukin 17 and regulatory T-cell induction. The gene discussed is IL17A; the disease is infection.