ABSTRACT
Granulomatous inflammation is a reaction to ongoing antigen presentation, and the control of that granuloma will have a critical impact on tissue pathology and therefore the course of the disease. Cessation of the antigenic stimulation will lead to cessation of the inflammatory response, with cell apoptosis occurring passively in response to cytokine withdrawal. However, apoptosis can be active also, and these pathways have attracted attention as dysregulation of apoptosis could potentially contribute to pathological granulomatous inflammation. The TNF-receptor (TNF-R) and TNF-ligand (TNF-L) superfamilies may be dysregulated in certain fibrotic lung diseases, including sarcoidosis.72
