The expression of microvesicles in the blood of patients with Graves' disease and its relationship to treatment.

Published

Journal Article

OBJECTIVE: Graves' disease (GD) is an autoimmune disease characterized by the presence of circulating autoantibodies against thyroid-stimulating hormone (TSH) receptor. Despite extensive research, the pathogenic mechanisms remain unclear. Immune responses associated with the disease may lead to cell activation/apoptosis and the release of microvesicles (MVs) into the circulation. MVs can display biological activities which may aggravate GD further. We studied immune mechanisms in GD by investigating the numbers and phenotype of circulating MVs in patients before and after antithyroid therapy with thiamazole. PATIENTS AND MEASUREMENTS: Samples were obtained from 15 patients with GD in the acute phase of hyperthyroidism and following 17-26 months treatment and 14 healthy controls. MVs from platelets, endothelial cells and monocytes exposing inflammation/activation markers (P-selectin, CD40 ligand, E-selectin and HMGB1) and MVs containing nuclear molecules were measured with flow cytometry. RESULTS: Patients had elevated baseline values of MVs (P < 0·001 for all types of MVs), while the levels decreased during thiamazole treatment (P < 0·05 for all types of MVs). The majority of MV populations remained, however, significantly higher in patients after treatment compared to levels in controls. CONCLUSIONS: GD patients have elevated levels of MVs that carry molecules with potential biological activities. MVs are significantly reduced after antithyroid treatment with thiamazole but still higher compared to levels in healthy controls. Assessment of MV levels and pattern may therefore provide additional information on underlying immune disturbances not obtained by measurements of hormone levels alone.

Full Text

Duke Authors

Cited Authors

  • Mobarrez, F; Abraham-Nordling, M; Aguilera-Gatica, K; Friberg, I; Antovic, A; Pisetsky, DS; Jörneskog, G; Wallen, H

Published Date

  • May 2016

Published In

Volume / Issue

  • 84 / 5

Start / End Page

  • 729 - 735

PubMed ID

  • 26252432

Pubmed Central ID

  • 26252432

Electronic International Standard Serial Number (EISSN)

  • 1365-2265

Digital Object Identifier (DOI)

  • 10.1111/cen.12872

Language

  • eng

Conference Location

  • England