In old age the majority of thyroid peroxidase autoantibodies are directed to a single TPO domain irrespective of thyroid function and iodine intake

• Published in: Clinical endocrinology (Oxford) 1998-06, Vol.48 (6), p.803-808
• Main Authors: Czarnocka, Barbara, Szabolcs, István, Pastuszko, Danuta, Feldkamp, Joachim, Dohán, Orsolya, Podoba, Jan, Wenzel, Bjorn
• Format: Article
• Language: English
• Subjects: Aged; Aged, 80 and over; Aging - immunology; Antibodies, Monoclonal - metabolism; Autoantibodies - immunology; Binding, Competitive; Biological and medical sciences; Epitopes - immunology; Fundamental and applied biological sciences. Psychology; Hormones. Regulation; Humans; Hypothyroidism - immunology; Iodide Peroxidase - immunology; Iodine - administration & dosage; Thyroid. Parathyroid. Ultimobranchial body; Vertebrates: endocrinology
• ISSN: 0300-0664; 1365-2265
• DOI: 10.1046/j.1365-2265.1998.00467.x

OBJECTIVE We have examined (1) which epitopes on thyroid peroxidase (TPO) are recognized by TPO autoantibodies (TPO‐Aab) in old age and to what extent? (2) Does the TPO‐Aab pattern differ in euthyroid and hypothyroid elderly subjects or does it depend on their iodine intake? DESIGN TPO‐Aab positive sera obtained from a screening study of nursing‐home residents living in areas of varying iodine intake were tested by competition studies with monoclonal antibodies (mAbs) recognizing different epitopes on TPO. SUBJECTS The nursing‐home residents with TPO‐Aab positivity were from (A) an iodine abundant area (Eastern Hungary, median iodine excretion ‐MIE‐: 0.462 μmol/mmol creatinine, N = 13); (B) an area of obligatory iodinated salt prophylaxis since the 1950s (Slovakia, MIE: 0.090 μmol/mmol creatinine, N = 11); (C) a moderately iodine‐deficient area (Northern Hungary, MIE: 0.065 μmol/mmol creatinine, N = 13). MEASUREMENTS Thirteen murine TPO antibodies generated against several epitopes of the four (A, B, C, D) antigenic domains on the TPO were co‐incubated with the TPO‐Aab positive sera on TPO coated microtitre plates. The amount of mAb bound was estimated after further incubation with goat anti‐mouse antibodies, conjugated with horseradish peroxidase and tetramethylbenzidine as chromogen. The TPO‐Aab positive sera were characterized by the pattern of percen_tage of inhibition of mAb binding caused by the TPO‐Aabs. RESULTS TPO‐Aabs inhibited only the binding of mAbs raised against the antigenic domains A (mAb9, mAb2, mAb60) and B (mAb64, mAb59, mAb18, mAb15). The extent of inhibition depended upon the TPO‐Aab titre but in all cases the binding of mAb9 was inhibited to the highest degree. The percen_tage inhibition of mAb9 was (a) 34 ± 17% (M ± SD) caused by sera (N = 8) with TPO‐Aab titre 1/100–1/200 (higher than that of all mAbs recognizing domain B, P