Rarity of anti- Na+/I- symporter (NIS) antibody with iodide uptake inhibiting activity in autoimmune thyroid diseases (AITD).

Citation
Hs. Chin et al., Rarity of anti- Na+/I- symporter (NIS) antibody with iodide uptake inhibiting activity in autoimmune thyroid diseases (AITD)., J CLIN END, 85(10), 2000, pp. 3937-3940
Citations number
16
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
ISSN journal
0021972X → ACNP
Volume
85
Issue
10
Year of publication
2000
Pages
3937 - 3940
Database
ISI
SICI code
0021-972X(200010)85:10<3937:ROANS(>2.0.ZU;2-B
Abstract
The search for antibody against the Na+/I- symporter (NIS) has seen conflic ting results over the years. Prior to cloning of NIS, Raspe et al found iod ide uptake inhibiting sera were rare in autoimmune thyroid diseases (AITD) while post-cloning, others reported the presence of antibody in 12-15% of H ashimoto's thyroiditis (HT) and 30-84% of Graves' disease (GD). To evaluate the role of NIS as a potential antigen in AITD, a stable COS 7 cell line e xpressing high level of functional hNIS was established which allowed the s creening of large number of sera for iodide uptake inhibiting activity in a 96-well plate format. Five hundred and fourteen serum samples taken from n ormal subjects and patients with AITD, non-autoimmune thyroid diseases, and non-thyroid autoimmune diseases were assayed for presence of iodide uptake inhibiting activity. Under the influence of these sera, iodide uptake show ed a normal frequency distribution and diminution of uptake 2 SDs below the mean of controls was observed with 14 sera. Among these, 7 that were avail able for further study were re-evaluated after dialysis and/or Ig G extract ion. All 7 sera lost their iodide uptake inhibiting activity, indicating th at the effects were not antibody mediated and unknown serum factors had bee n responsible. In conclusion, contrary to previous results, the present stu dy indicates that antibodies capable of modulating NIS activity are rare in AITD.