Apoptosis of NOD.H2 h4 thyrocytes by low concentrations of iodide is associated with impaired control of oxidative stress.

ABSTRACT:

Background

Enhanced iodide intake in NOD.H2(h4) mice accelerates the incidence and severity of spontaneous autoimmune thyroiditis (SAT) via an unknown mechanism. A plausible hypothesis is that iodide-induced apoptosis of thyrocytes can create imbalances in antigenic load and/or disruption of immunoregulatory mechanisms that facilitate activation of autoreactive T cells in cervical lymph nodes draining the thyroid.

Methods

We examined whether NOD.H2(h4) thyrocytes, exposed to low NaI concentrations in vitro, are more susceptible to apoptosis compared to thyrocytes from CBA/J mice, which are resistant to iodide-accelerated SAT (ISAT). We also looked, at the transcriptional level, for differential activation of genes involved in apoptosis or oxidative stress pathways that may a

SUBMITTER: Kolypetri P 

PROVIDER: S-EPMC4080865 | biostudies-literature | 2014 Jul

REPOSITORIES: biostudies-literature