With the data that are currently available, our perspective is that chronic fibrosis in sarcoidosis is likely to be driven by a combination of increased Th17 cells, possibly due to resistance to apoptosis, combined with primed monocyte-derived macrophages (TLR3 polymorphism, type 1 IFN signalling) which may respond disproportionately to infection (acute, low grade or the microbiome) (summarised in table 2). This evidence concerns the gene TLR3 and fibrosis.