TY - JOUR
T1 - Iodine and IFN-γ synergistically enhance intercellular adhesion molecule 1 expression on NOD.H2h4 mouse thyrocytes
AU - Sharma, Rajni B.
AU - Alegria, Judy D.
AU - Talor, Monica V.
AU - Rose, Noel R.
AU - Caturegli, Patrizio
AU - Burek, C. Lynne
PY - 2005/6/15
Y1 - 2005/6/15
N2 - NOD.H2h4 mice spontaneously develop autoimmune lymphocytic thyroiditis that mimics human Hashimoto's thyroiditis, a disease where iodine, IFN-γ, and adhesion molecules have all been implicated in the pathogenesis. To study how iodine and IFN-γ modulate the expression of ICAM-1, we analyzed NOD.H2h4 thyrocytes in baseline conditions (day 0) and at several time points following supplementation of iodine in the drinking water. On day 0, a small percentage (∼10%) of thyrocytes constitutively expressed ICAM-1. The expression gradually increased to 13, 25, and 41% on days 7, 14 and 28, respectively, returning to baseline (9%) on day 35. The initial ICAM-1 kinetics was paralleled by thyroidal infiltration of CD45+ hemopoietic cells, which increased from an average of 4% on day 0 to an average of 13, 21, and 24% on days 14, 28, and 35, respectively. To distinguish whether the observed ICAM-1 increase was a direct effect of iodine or a consequence of the immune infiltrate, we treated mouse primary thyrocyte cultures with 0.01 mM sodium iodine and showed a 3-fold increased ICAM-1 expression. To assess interaction between IFN-γ and iodine, we analyzed CD45 and ICAM-1 expression on thyrocytes from NOD.H2h4 wild-type and NOD.H2h4 thyr-IFN-γ transgenic littermates. Strikingly, IFN-γ interacted synergistically with iodine to enhance ICAM-1 expression on thyrocytes. These findings suggest that iodine and IFN-γ cooperate to promote thyroidal expression of ICAM-1 in this mouse model of thyroiditis, highlighting the complex interplay present in the pathogenesis of Hashimoto's thyroiditis.
AB - NOD.H2h4 mice spontaneously develop autoimmune lymphocytic thyroiditis that mimics human Hashimoto's thyroiditis, a disease where iodine, IFN-γ, and adhesion molecules have all been implicated in the pathogenesis. To study how iodine and IFN-γ modulate the expression of ICAM-1, we analyzed NOD.H2h4 thyrocytes in baseline conditions (day 0) and at several time points following supplementation of iodine in the drinking water. On day 0, a small percentage (∼10%) of thyrocytes constitutively expressed ICAM-1. The expression gradually increased to 13, 25, and 41% on days 7, 14 and 28, respectively, returning to baseline (9%) on day 35. The initial ICAM-1 kinetics was paralleled by thyroidal infiltration of CD45+ hemopoietic cells, which increased from an average of 4% on day 0 to an average of 13, 21, and 24% on days 14, 28, and 35, respectively. To distinguish whether the observed ICAM-1 increase was a direct effect of iodine or a consequence of the immune infiltrate, we treated mouse primary thyrocyte cultures with 0.01 mM sodium iodine and showed a 3-fold increased ICAM-1 expression. To assess interaction between IFN-γ and iodine, we analyzed CD45 and ICAM-1 expression on thyrocytes from NOD.H2h4 wild-type and NOD.H2h4 thyr-IFN-γ transgenic littermates. Strikingly, IFN-γ interacted synergistically with iodine to enhance ICAM-1 expression on thyrocytes. These findings suggest that iodine and IFN-γ cooperate to promote thyroidal expression of ICAM-1 in this mouse model of thyroiditis, highlighting the complex interplay present in the pathogenesis of Hashimoto's thyroiditis.
UR - http://www.scopus.com/inward/record.url?scp=20444382456&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=20444382456&partnerID=8YFLogxK
U2 - 10.4049/jimmunol.174.12.7740
DO - 10.4049/jimmunol.174.12.7740
M3 - Article
C2 - 15944276
AN - SCOPUS:20444382456
SN - 0022-1767
VL - 174
SP - 7740
EP - 7745
JO - Journal of Immunology
JF - Journal of Immunology
IS - 12
ER -