Mass Cytometry Studies of Patients With Autoimmune Endocrine Diseases Reveal Distinct Disease-Specific Alterations in Immune Cell Subsets

Although there is evidence that autoimmune diseases share similar immunogenetic mechanisms, studies comparing peripheral CD45(+) cells from patients with autoimmune endocrine diseases in parallel are limited. In this study, we applied high-dimensional single-cell mass cytometry to phenotypically characterize PBMC from patients with new-onset (N-T1D) and long-standing type 1 diabetes, Hashimoto's thyroiditis (HT), Graves' disease and autoimmune Addison's disease (AD), as well as healthy controls. The frequency of CD20(lo)CD27(hi)CD38(hi)HLA-DR(int) plasmablasts, CD86(+)CD14(lo)CD16(+) non-classical monocytes and two subsets of CD56(dim)HLA-DR(+)IFN-γ(+) NK cells were increased in patients with HT. Subsets of CD56(dim)CD69(+)HLA-DR(−) NK cells and CD8(+) TEMRA cells, both expressing IFN-γ, were expanded and reduced, respectively, in the N-T1D group. In addition, patients with AD were characterized by an increased percentage of central memory CD8(+) T cells that expressed CCR4, GATA3, and IL-2. We demonstrate that patients with N-T1D, HT, and AD had altered frequencies of distinct subsets within antigen-presenting and cytotoxic cell lineages. Previously unreported alterations of specific cell subsets were identified in samples from patients with HT and AD. Our study might contribute to a better understanding of shared and diverging immunological features between autoimmune endocrine diseases.