ArticleClinical and experimental immunology2014
The effect of types I and III interferons on adrenocortical cells and its possible implications for autoimmune Addison's disease.
Article in Clinical and experimental immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Transcriptional regulation and signaling of type IV interferon in Carassius gibelio.Cell communication and signaling : CCS · 2025Article
- The potential role for infections in the pathogenesis of autoimmune Addison's disease.Clinical and experimental immunology · 2019Review
- Impact of Month of Birth on the Risk of Development of Autoimmune Addison's Disease.The Journal of clinical endocrinology and metabolism · 2016Article
- Analysis of cellular and humoral immune responses against cytomegalovirus in patients with autoimmune Addison's disease.Journal of translational medicine · 2016Article
- Polymorphisms of the Toll-Like Receptor-3 Gene in Autoimmune Adrenal Failure and Type 1 Diabetes in Polish Patients.Archivum immunologiae et therapiae experimentalis · 2016Article
- Peripheral Blood Cells from Patients with Autoimmune Addison's Disease Poorly Respond to Interferons In Vitro, Despite Elevated Serum Levels of Interferon-Inducible Chemokines.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2015Article
- Type I IFN family members: similarity, differences and interaction.Cytokine & growth factor reviews · 2015Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autoimmune Addison's disease (AAD) is caused by selective destruction of the hormone-producing cells of the adrenal cortex. As yet, little is known about the potential role played by environmental factors in this process. Type I and/or type III interferons (IFNs) are signature responses to virus infections, and have also been implicated in the pathogenesis of autoimmune endocrine disorders such as type 1 diabetes and autoimmune thyroiditis. Transient development of AAD and exacerbation of established or subclinical disease, as well as the induction of autoantibodies associated with AAD, have been reported following therapeutic administration of type I IFNs. We therefore hypothesize that exposure to such IFNs could render the adrenal cortex susceptible to autoimmune attack in genetically predisposed individuals. In this study, we investigated possible immunopathological effects of type I and type III IFNs on adrenocortical cells in relation to AAD. Both types I and III IFNs exerted significant cytotoxicity on NCI-H295R adrenocortical carcinoma cells and potentiated IFN-γ- and polyinosine-polycytidylic acid [poly (I : C)]-induced chemokine secretion. Furthermore, we observed increased expression of human leucocyte antigen (HLA) class I molecules and up-regulation of 21-hydroxylase, the primary antigenic target in AAD. We propose that these combined effects could serve to initiate or aggravate an ongoing autoimmune response against the adrenal cortex in AAD.
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