More evidence that sarcoidosis is a host disease, and the identity of the aetiological triggers is irrelevant
European Respiratory Journal 2024 64(6): 2402051; DOI: https://doi.org/10.1183/13993003.02051-2024
Extract
Conventionally, sarcoidosis has been understood to be a dysfunctional immune response to an inciting antigen(s) in a previously “normal” individual. There are clearly pre-existing genetic, epigenetic and exposure factors that modify the chance of manifesting sarcoidosis, but epidemiological data that suggest transmissibility have reinforced the notion that a mysterious agent must be foisting granulomatous inflammation on unsuspecting but susceptible individuals unfortunate enough to be in the wrong place at the wrong time. In a famous example, spatial and temporal clusters of sarcoidosis in unrelated individuals were documented over a 20-year period on the Isle of Man [1]. Other observations also suggest an exogenous trigger, including transmission by organ transplantation and events such as the World Trade Center disaster [2, 3]. This prevailing conceptual framework, therefore, has resulted in an intense search for the identity and properties of the elusive antigenic triggers.
