Inanti-neutrophil cytoplasmic autoantibody-associated vasculitides (AAV), severalobservations support a key role of T-helper cells (CD4 + T cells) in disease pathophysiology. An expanded populationof effector memory CD4 + T cells in AAVpatients may contribute to tissue injury and disease progression. In addition,functional impairment of regulatory T cells (T Regs) is reported in AAV patients. A fraction of T Regs have the capacity to differentiate into Th17 cells in the contextof a proinflammatory environment. Therefore, nonfunctionality of T Regs described in AAV patients may be caused by their conversioninto IL-17-producing cells that may contribute to granulomatous vasculitis.Further investigations directed at the plasticity of T Regs in AAV patients are warranted.