Sarcoidosis is a chronic multisystemic granulomatous disorder thought to result from an exaggerated cellular immune response to a variety of self antigens or non-self antigens.1 The aetiology of sarcoidosis is unknown, which might be in part related to the diverse manifestations of the disease and the absence of approved diagnostic criteria. Although specific inhalation antigens have been put forward as possible triggers, no study has yet proved a consistent relation with a causative agent.2 Genetic factors might also be involved since familial incidence in certain populations as high as 19% has been noted and, further, specific HLA associations have been connected with disease susceptibility and outcome—for example, HLA-B8 and DR-3 with Löfgren's syndrome (acute systemic disease with fever, polyarthritis, erythema nodosum, and favourable prognosis).3 4 The infectious agents, specifically mycobacteria and more recently herpesvirus 8, have also been implicated.5 6 Sarcoidosis has only sporadically been reported in AIDS and has occasionally been described during the immune recovery with the highly active antiretroviral therapy.7 8 The evidence that disease might be of environmental or infectious origin is supported by occupational clustering (medical nurses, fire fighters) and by the transmission of the disease from transplanted organs.9-11 The genetic and environmental influences cannot be adequately evaluated in small samples of patients; a large study addressing the phenotyping differences and various environmental data is lacking however. So far, only interesting disease patterns in families and inconclusive allelic associations for different populations have been reported. Therefore, sarcoidosis might represent an abnormal immune response directed against one or more possible antigens in an individual with a hereditary or acquired abnormality of the immune system.