title: Lower proportions of CD4+CD25(high) and CD4+FoxP3, but not CD4+CD25+CD127(low) FoxP3+ T cell levels in children with autoimmune thyroid diseases.
abstract: The essence of autoimmune thyroid disease (AITD) is loss of tolerance of own tissues caused by malfunction of T lymphocytes, which affects the production of antibodies reacting with particular cell structures and tissues. Foxp3(+) regulatory T cells (Tregs) take part in the regulation of immune response and play a leading role in developing immune tolerance through active suppression. The aim of the study was to estimate the expression of CD4+CD25(high), CD4+CD25+CD127(low)FoxP3(+) and CD4+ FoxP3 T cells in patients with Graves' disease (GD) (n = 24, median age 15.5 years), in patients with Hashimoto's thyroiditis (HT) (n = 30, median age 15 years) in comparison with sex- and age-matched healthy control subjects (n = 30, median age 15 years). Polychromatic flow cytometry using a FACSCalibur (BD Biosciences) cytometer was applied to delineate T regulatory cell populations. In untreated patients with Graves' disease and HT we observed a significant decrease in CD4+FoxP3 (p < 0.001, p < 0.01) and CD4+CD25(high) (p < 0.016, p < 0.048) T lymphocytes as compared to the healthy control subjects. After 6-12 months of L-thyroxine therapy in HT cases these phenotypes of Tregs were normalized, yet no such changes were observed during GD therapy. The analysis of CD4+CD25+CD127(low)FoxP3+ T cells in the peripheral blood revealed comparable percentages of these cells in patients with thyroid autoimmune diseases to the controls. We conclude that the reduction number of Tregs with CD4+CD25(high) and CD4+FoxP3 phenotype suggests their role in initiation and development of autoimmune process in thyroid disorders.
authors.affiliation: Department of Pediatrics Endocrinology, Diabetology with Cardiology Division, Medical University of Bialystok, Poland. abossowski@hotmail.com
authors.forename: A
authors.initials: A
authors.lastname: Bossowski
authors.forename: M
authors.initials: M
authors.lastname: Moniuszko
authors.forename: M
authors.initials: M
authors.lastname: Dąbrowska
authors.forename: B
authors.initials: B
authors.lastname: Sawicka
authors.forename: M
authors.initials: M
authors.lastname: Rusak
authors.forename: M
authors.initials: M
authors.lastname: Jeznach
authors.forename: J
authors.initials: J
authors.lastname: Wójtowicz
authors.forename: A
authors.initials: A
authors.lastname: Bodzenta-Lukaszyk
authors.forename: A
authors.initials: A
authors.lastname: Bossowska
mesh_terms: D000293:Adolescent; D015704:CD4 Antigens / Q000378:metabolism; D002648:Child; D005260:Female; D051858:Forkhead Transcription Factors / Q000378:metabolism; D006111:Graves Disease / Q000276:immunology*; D050031:Hashimoto Disease / Q000276:immunology*; D006801:Humans; D053645:Interleukin-2 Receptor alpha Subunit / Q000378:metabolism; D053699:Interleukin-7 Receptor alpha Subunit / Q000378:metabolism; D008297:Male; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D013961:Thyroid Gland / Q000276:immunology; D013974:Thyroxine / Q000627:therapeutic use*; D055815:Young Adult
chemical_list: D015704:CD4 Antigens; C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; D053645:Interleukin-2 Receptor alpha Subunit; D053699:Interleukin-7 Receptor alpha Subunit; D013974:Thyroxine