Get your full text copy in PDF
Alberto Gómez, Angela Umana, Alba Alicia Trespalacios
Med Sci Monit 2006; 12(3): BR103-113
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 prurigonor its etiological agent have been described. Not much is known about the pathogenic mechanisms of thedisease, although associations with the human leucocitary antigens (HLA) and local immune responses seemto play an important role in its expression, as is the case in other skin autoimmune disorders, suchas pemphigus and psoriasis. Material/Methods: In this paper we compare cellular and humoral immunitythrough in vitro proliferation studies, ELISA and immunofluorescence tests in actinic prurigo patientsand healthy controls. Results: Autoantibody reactivities on the skin and also proliferative responsesto isolated autologous skin antigens were higher in patients than in controls. The polyclonal cellularimmune response against T cell mitogens and against allogeneic stimuli was found to be diminished inpatients. Conclusions: We found autoimmune reactivity in patients suffering from actinic prurigo. Wepostulate 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 immuneresponse should be localized and the observed infiltrating lymphocytes in skin biopsies should be activatedby these hypothetical antigens.