Autoimmune Myasthenia Gravis (MG) is characterized by invalidating muscle weaknesses due especially to anti-acetylcholine receptor autoantibodies. As for other autoimmune diseases, immune dysregulations are well known for adaptive immune cells, such as B and T cells. However, to further gain insight into immune dysregulation underlying MG, we performed an in-depth analysis on peripheral mononuclear blood cells using mass cytometry. Cells from 24 AChR+ MG patients and 16 age- and sex-matched controls were stained with 37 antibodies and acquired on a Helios™ mass cytometer. Using both unsupervised and supervised approaches, we identified several circulating cell subpopulations whom expression was affected in MG, and that had not been previously associated with this disease. MG was associated with a reduction of circulating monocytes, for all subpopulations: classical (CD14++CD16-), intermediate (CD14+/++CD16+) and non-classical (CD14low CD16+) monocytes. In contrast, an increase in innate lymphoid cells 2 (ILC-2: CD161+CRTH2+) and of gδ T17 cells (gδ+CD27-) was observed in MG patients. This increase in gδ T17 cells was not detected in periphery by classical flow cytometry that might be less discriminative than mass cytometry but was clearly detected in thymic cells of MG patients. These analyses have unraveled unexpected dysregulations on innate immune cells and further investigations are ongoing to better understand their implication in MG. Innate immunity is crucial for host defense, but its improper activation could also be involved in autoimmunity.