In sarcoidosis, IL-10 release is inhibited by IFN-γ, thus allowing DCs to release proinflammatory cytokines and MMPs and contributing to tissue damage and disease progression.117Additionally, DC activate T cells, which stimulate macrophage differentiation into epithelioid and MGCs, further contributing to the granuloma core.118These reciprocal interactions between DCs and macrophages are central to granuloma organization and persistence, and their disruption may represent a key immunopathologic mechanism in sarcoidosis progression. This evidence concerns the gene IFNG and sarcoidosis.