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Updated: Dec 11, 2025

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
Published on: March 17, 2023
Quantitative and Functional Analysis of PD-1+ NK Cells in Patients With Autoimmune Thyroid Disease
Alma Cesleste Ortega-Rodríguez1, Rebeca Martínez-Hernández2, Adriana Monsiváis-Urenda1,3
1Section of Molecular and Translational Medicine, CICSaB, UASLP, San Luis Potosí, SLP, México.
Context:
Natural killer (NK) cells have an important role in innate immunity and in the regulation of immune response. The role of NK cells expressing the programmed cell death protein-1 (PD-1) regulatory receptor has not been explored in patients with autoimmune thyroid disease (AITD).
Purpose:
To analyze the levels and function of PD-1+ NK cells in samples from AITD patients.
Design:
Cases and controls, observational study.
Setting:
Hospital Universitario la Princesa, Spain.
Patients:
Forty patients with AITD, 16 with Hashimoto thyroiditis (HT), 24 with Graves' disease (GD), and 15 healthy controls.
Intervention:
Multiparametric flow cytometry analysis of peripheral blood NK cells. In vitro assays of cytotoxic activity of NK cells, and synthesis of cytokines.
Main Outcome Measures:
Levels and function of PD-1+ NK cells in blood samples from AITD patients and controls.
Results:
Increased levels of NK cells and the CD56dimPD-1+ subset were observed in GD patients. In HT, an enhanced expression of the regulatory receptors NKG2A and NKG2C by CD56brightPD-1+ NK cells was detected. AITD patients showed an increased synthesis of IL-10 by CD56brightPD-1- NK cells, whereas CD56dimPD-1+ cells from GD patients exhibited an enhanced production of interferon-γ. PD-1+ NK cells from patients with GD and HT showed an increased cytotoxic activity. Significant associations were observed in patients with GD or HT between the levels of PD-1+ NK cells and clinical laboratory parameters.
Conclusions:
The different abnormalities in NK cell subset levels, in the expression of PD-1 and its function in AITD patients' further support the complex role of these cells in this pathogenesis.

