Abstract
Despite that autoimmune diseases share similar immunogenetic mechanisms, studies comparing the protein composition in peripheral blood from patients with autoimmune endocrine diseases are limited. In this study, we applied proximity extension assay to measure proteins related to signaling and interactions within the immune system in peripheral blood from patients with new-onset (N-T1D) and long-standing (L-T1D) type 1 diabetes, Hashimoto's thyroiditis (HT), Graves' disease (GD), and autoimmune Addison's disease in addition to healthy controls (HC). Proteins in plasma and supernatants from cultured PBMC were measured by using a 92-plex Olink® INFLAMMATION panel. Soluble CDCP1 was more abundant in plasma from patients with N-T1D, L-T1D, HT, and GD than in HC. The L-T1D and HT groups had elevated plasma levels of SLAMF1 compared with HC. Patients and HC could not be distinguished by their protein composition in PBMC supernatants. The high-throughput multiplex technology enabled us to detect two low-abundant proteins that have been gradually connected to autoimmune diseases. Our study provides novel associations between CDCP1, SLAMF1, and autoimmune endocrine diseases, which might reflect a higher degree of inflammation and lymphocyte activation.
Highlights
The concepts “mosaic of autoimmunity” and “autoimmune tautology” declare that several features underlying autoimmunity are shared between diseases [1, 2]
By measuring cytokines and chemokines in various sample matrices, it has been hypothesized that type 1 diabetes (T1D), Hashimoto’s thyroiditis (HT), Graves’ disease (GD), and Addison’s disease (AD) are mainly mediated by pro-inflammatory and Th1-biased immune responses [8,9,10,11,12,13,14]
Plasma and supernatants from cultured PBMC were collected in order to compare the peripheral protein composition between patients with T1D, HT, GD, and AD as well as healthy controls (HC)
Summary
The concepts “mosaic of autoimmunity” and “autoimmune tautology” declare that several features underlying autoimmunity are shared between diseases [1, 2]. The proposed model pertains all autoimmune conditions, genetic, hormonal, immunological, and environmental factors can interact differently and determine the final disease. HT and GD are autoimmune diseases of the thyroid gland that cause hypo- and hyperthyroidism, respectively. The loss of aldosterone and cortisol production in AD is caused by immune-mediated destruction within the Plasma Proteins in Endocrine Autoimmunity adrenal glands. By measuring cytokines and chemokines in various sample matrices, it has been hypothesized that T1D, HT, GD, and AD are mainly mediated by pro-inflammatory and Th1-biased immune responses [8,9,10,11,12,13,14]. A limited number of analytes have been assessed despite that immune responses comprise a complex network of protein interactions
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