Therefore, preferential crosstalk between NLRC4 with FcγRs such as CD64 might drive inflammasome-mediated inflammatory responses to intracellular dsDNA and IgG complexes in CD1c+ cDC from patients with RA while interactions between this and other inflammasome sensors are required to acquire Th17-activating functional abilities. This evidence concerns the gene CD1C and rheumatoid arthritis.