We found altered receptor–ligand pairing between CD14+ or CD16+ monocytes and cDCs other than pDCs (Fig. 5f), suggesting that the differentiation of circulating monocytes into cDCs might be modulated through TNF signaling and TGF-β signaling and the cDCs derived from monocytes might be with different phenotypes and functional profiles in MG patients. This evidence concerns the gene FCGR3A and myasthenia gravis.