title: Sarcoidosis and molecular mimicry--important etiopathogenetic aspects: current state and future directions.
abstract: Sarcoidosis is a disease of uncertainty in terms of its cause, presentation, and clinical course. The disease has a worldwide distribution and affects all ages, races, and both sex. Sarcoidosis of the skin may have an extremely heterogeneous clinical presentation, so that the definitions of 'great imitator' and 'clinical chameleon' have long been used. The factors that influence clinical picture and severity of the disease are probably linked to the etiopathogenesis of sarcoidosis, which continues to be shrouded in mystery. The current state of the art on the pathogenesis of sarcoidosis is that it is an immunological response in a genetically susceptible individual to an as-yet undefined antigenic stimulus. How exposure occurs in genetically predisposed patients is not completely clear, but the most likely explanation is that these agents or antigens are either inhaled into the lungs or enter through contact with the skin, as these are the common target organs that are constantly in contact with the environment. An autoimmune etiology of sarcoidosis could possibly occur through a process of molecular mimicry of infectious or other environmental antigens to host antigens. This could lead to a cross-mediated immune response and induction of autoimmune disease. This molecular mimicry may probably be responsible for the heterogeneous clinical presentations of the disease. Several investigations and studies have provided valuable evidence on the etiopathogenesis of sarcoidosis, which may lead to the future development of targeted and innovative treatment strategies. Nevertheless, we are still a long way from unravelling the underlying cause of this mysterious disease.
authors.affiliation: Policlinic for Dermatology and Venereology, University Hospital Lozenetz, Academic Educational Hospital of The Saint Kliment Ohridski University, Koziak street 1, 1407, Sofia, Bulgaria. georgi_tchernev@yahoo.de
authors.forename: Georgi
authors.initials: G
authors.lastname: Tchernev
authors.forename: Julian
authors.initials: J
authors.lastname: Ananiev
authors.forename: José Carlos
authors.initials: JC
authors.lastname: Cardoso
authors.forename: Uwe
authors.initials: U
authors.lastname: Wollina
authors.forename: Shyam B
authors.initials: SB
authors.lastname: Verma
authors.forename: James W
authors.initials: JW
authors.lastname: Patterson
authors.forename: Lyubomir A
authors.initials: LA
authors.lastname: Dourmishev
authors.forename: Michael
authors.initials: M
authors.lastname: Tronnier
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Okamoto
authors.forename: Kana
authors.initials: K
authors.lastname: Mizuno
authors.forename: Nobuo
authors.initials: N
authors.lastname: Kanazawa
authors.forename: Maya
authors.initials: M
authors.lastname: Gulubova
authors.forename: Irena
authors.initials: I
authors.lastname: Manolova
authors.forename: Cristina
authors.initials: C
authors.lastname: Salaro
mesh_terms: D006801:Humans; D007113:Immunity, Innate / Q000235:genetics* / Q000276:immunology*; D008957:Models, Genetic; D018448:Models, Immunological; D018716:Molecular Mimicry / Q000235:genetics* / Q000276:immunology*; D012507:Sarcoidosis / Q000503:physiopathology*