The effect of types I and III interferons on adrenocortical cells and its possible implications for autoimmune Addison's disease

摘要: Autoimmune Addison's disease (AAD) is caused by selective destruction of the hormone-producing cells adrenal cortex. As yet, little known about potential role played environmental factors in this process. Type I and/or type III interferons (IFNs) are signature responses to virus infections, and have also been implicated pathogenesis autoimmune endocrine disorders such as 1 diabetes thyroiditis. Transient development AAD exacerbation established or subclinical disease, well induction autoantibodies associated with AAD, reported following therapeutic administration IFNs. We therefore hypothesize that exposure IFNs could render cortex susceptible attack genetically predisposed individuals. In study, we investigated possible immunopathological effects on adrenocortical relation AAD. Both types exerted significant cytotoxicity NCI-H295R carcinoma potentiated IFN-γ-and polyinosine-polycytidylic acid [poly (I : C)]-induced chemokine secretion. Furthermore, observed increased expression human leucocyte antigen (HLA) class molecules up-regulation 21-hydroxylase, primary antigenic target propose these combined serve initiate aggravate an ongoing response against