Endocrine Abstracts

Autoimmune Addison’s disease (AAD) is an endocrine disease resulting from the immune system’s destruction of hormone producing cells in the adrenal cortex. Autoantibodies against the steroidogenic enzyme 21-hydroxylase (21OH) is the hallmark of this form, and found in about 85 percent of patients in European populations. Risk factors are both genetic and presumably environmental. Genes associated with AAD are MHC class II especially the DR locus, MHC class I and MIC-A, but other immune genes such as PTPN22 and CTLA-4 also contribute.

Recently, T cells reactivities against 21OH have been observed in patients with AAD, all of which had autoantibodies against 21OH. Moreover, the high-risk genotype DR3/DR4(0404) was frequently observed among those showing T cell proliferation. Autoantibodies potentiated the proliferative response and epitope mapping revealed that the peptide 21OH(342–361) was responsible for much of the reactivity. The adrenocortical cell itself may participate in the autoimmune destruction by expressing toll-like receptors and producing chemokines such as interferon inducible protein 10 thereby attracting lymphocytes to the adrenal cortex.

We hypothesized that the hormone producing cells in the adrenal cortex under proinflammatory conditions, such as viral infections, play a critical part in the induction of autoimmune Addison’s disease in genetically susceptible individuals.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details are unavailable.