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Activation of thyroid antigen-reactive B cells in recent onset autoimmune thyroid disease patients.
Smith, Mia J; Rihanek, Marynette; Coleman, Brianne M; Gottlieb, Peter A; Sarapura, Virginia D; Cambier, John C.
Afiliação
  • Smith MJ; Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO, USA; Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, CO, USA.
  • Rihanek M; Barbara Davis Center for Childhood Diabetes, University of Colorado School of Medicine, Aurora, CO, USA.
  • Coleman BM; Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO, USA.
  • Gottlieb PA; Barbara Davis Center for Childhood Diabetes, University of Colorado School of Medicine, Aurora, CO, USA.
  • Sarapura VD; Division of Endocrinology, Metabolism, and Diabetes, University of Colorado Health Sciences Center, Aurora, CO, USA.
  • Cambier JC; Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO, USA. Electronic address: John.Cambier@ucdenver.edu.
J Autoimmun ; 89: 82-89, 2018 05.
Article em En | MEDLINE | ID: mdl-29233566
Autoimmune thyroid disease (AITD), including Hashimoto's thyroiditis (HT) and Graves' disease (GD), is the most common autoimmune disorder in the United States, affecting over 20 million people. At the time of diagnosis, both HD and GD are characterized by the accumulation of B and T lymphocytes in the thyroid gland and production of autoantibodies targeting the thyroid, indicating that a breach in tolerance of autoreactive lymphocytes has occurred. However, few studies have sought to understand the underlying pathogenesis of AITD that ultimately leads to production of autoantibodies and loss of thyroid function. In this study, we analyzed the phenotype of thyroid antigen-reactive B cells in the peripheral blood of recent onset and long standing AITD patients. We found that in recent onset patients thyroid antigen-reactive B cells in blood no longer appear anergic, rather they express CD86, a marker of activation. This likely reflects activation of these cells leading to their production of autoantibodies. Hence, this study reports the early loss of anergy in thyroid antigen-reactive B cells, an event that contributes to development of AITD.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Glândula Tireoide / Tireoidite Autoimune / Linfócitos B / Linfócitos T / Doença de Graves Limite: Female / Humans / Male Idioma: En Ano de publicação: 2018 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Glândula Tireoide / Tireoidite Autoimune / Linfócitos B / Linfócitos T / Doença de Graves Limite: Female / Humans / Male Idioma: En Ano de publicação: 2018 Tipo de documento: Article