Alberto Gómez1, Angela Umana, Alba Alicia Trespalacios. 1. Instituto de Genética Humana, Facultad de Medicina, Bogotá and Facultad de Ciencias, Pontificia Universidad Javeriana, Bogotá, Colombia. agomez@javeriana.edu.co
Abstract
BACKGROUND: Actinic prurigo (AP) is a frequent photodermatosis among Amerindians, with a high incidence among women and children below ten years of age. Neither the cause of actinic prurigo nor its etiological agent have been described. Not much is known about the pathogenic mechanisms of the disease, although associations with the human leucocitary antigens (HLA) and local immune responses seem to play an important role in its expression, as is the case in other skin autoimmune disorders, such as pemphigus and psoriasis. MATERIAL/ METHODS: In this paper we compare cellular and humoral immunity through in vitro proliferation studies, ELISA and immunofluorescence tests in actinic prurigo patients and healthy controls. RESULTS: Autoantibody reactivities on the skin and also proliferative responses to isolated autologous skin antigens were higher in patients than in controls. The polyclonal cellular immune response against T cell mitogens and against allogeneic stimuli was found to be diminished in patients. CONCLUSIONS: We found autoimmune reactivity in patients suffering from actinic prurigo. We postulate that AP patients may have one or more skin antigens that stimulate an autoimmune response, which causes the observed skin lesions. As AP is a pathology that affects mainly the skin, any immune response should be localized and the observed infiltrating lymphocytes in skin biopsies should be activated by these hypothetical antigens.
BACKGROUND:Actinic prurigo (AP) is a frequent photodermatosis among Amerindians, with a high incidence among women and children below ten years of age. Neither the cause of actinic prurigo nor its etiological agent have been described. Not much is known about the pathogenic mechanisms of the disease, although associations with the human leucocitary antigens (HLA) and local immune responses seem to play an important role in its expression, as is the case in other skin autoimmune disorders, such as pemphigus and psoriasis. MATERIAL/ METHODS: In this paper we compare cellular and humoral immunity through in vitro proliferation studies, ELISA and immunofluorescence tests in actinic prurigopatients and healthy controls. RESULTS: Autoantibody reactivities on the skin and also proliferative responses to isolated autologous skin antigens were higher in patients than in controls. The polyclonal cellular immune response against T cell mitogens and against allogeneic stimuli was found to be diminished in patients. CONCLUSIONS: We found autoimmune reactivity in patients suffering from actinic prurigo. We postulate that AP patients may have one or more skin antigens that stimulate an autoimmune response, which causes the observed skin lesions. As AP is a pathology that affects mainly the skin, any immune response should be localized and the observed infiltrating lymphocytes in skin biopsies should be activated by these hypothetical antigens.