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CD25+CD4+ regulatory T cells in patients with Kawasaki disease
Authors:Furuno Kenji  Yuge Tetsuji  Kusuhara Koichi  Takada Hidetoshi  Nishio Hisanori  Khajoee Vahid  Ohno Takuro  Hara Toshiro
Institution:Department of Pediatrics, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. furuken@pediatr.med.kyushu-u.ac.jp
Abstract:OBJECTIVE: To investigate whether the CD25 + CD4 + regulatory T-cell population, which plays important roles not only in maintaining immunologic self-tolerance but also in controlling the magnitude and character of antimicrobial immune responses, is related to the pathophysiology of Kawasaki disease (KD). STUDY DESIGN: The patient group consisted of 54 patients (median age, 30 months; 27 female and 27 male patients) fulfilling the criteria for KD. Age-matched control subjects included 17 patients with active infections and 24 healthy children. We analyzed CD25 + CD4 + cells and the mRNA expression of Foxp3, cytotoxic T lymphocyte-associated antigen 4 (CTLA4), glucocorticoid-induced tumor necrosis factor receptor (GITR), and transforming growth factor beta in peripheral blood mononuclear cells and purified CD4 + T cells. RESULTS: The proportions of CD25 + CD4 + cells in patients with acute-phase KD (median, 2.35% of total lymphocytes) were significantly lower than those in healthy control subjects (median, 3.14%) and control subjects with disease (median, 3.15%). The proportions returned to the normal level after intravenous gammaglobulin treatment (median, 3.86%). The mRNA expression of Foxp3, CTLA4, and GITR showed similar tendencies. CONCLUSIONS: The decrease of CD25 + CD4 + regulatory T cells in the acute phase might have a role in the development of KD.
Keywords:CTLA4  Cytotoxic T lymphocyte-associated antigen 4  GITR  Glucocorticoid-induced tumor necrosis factor receptor  IL  Interleukin  IVIG  Intravenous immunoglobulin  KD  Kawasaki disease  MNC  Mononuclear cell  SCID  Severe combined immunodeficiency  TGF-β  Transforming growth factor β
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