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      Circulating CXCR5+PD-1+ICOS+ Follicular T Helper Cells Are Increased Close to the Diagnosis of Type 1 Diabetes in Children With Multiple Autoantibodies.

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          Abstract

          Although type 1 diabetes (T1D) is primarily perceived as a T cell-driven autoimmune disease, islet autoantibodies are the best currently available biomarker for autoimmunity and disease risk. These antibodies are produced by autoreactive B cells, the activation of which is largely dependent on the function of CD4+CXCR5+ follicular T helper cells (Tfh). In this study, we have comprehensively characterized the Tfh- as well as B-cell compartments in a large cohort of children with newly diagnosed T1D or at different stages of preclinical T1D. We demonstrate that the frequency of CXCR5+PD-1+ICOS+-activated circulating Tfh cells is increased both in children with newly diagnosed T1D and in autoantibody-positive at-risk children with impaired glucose tolerance. Interestingly, this increase was only evident in children positive for two or more biochemical autoantibodies. No alterations in the circulating B-cell compartment were observed in children with either prediabetes or diabetes. Our results demonstrate that Tfh activation is detectable in the peripheral blood close to the presentation of clinical T1D but only in a subgroup of children identifiable by positivity for multiple autoantibodies. These findings suggest a role for Tfh cells in the pathogenesis of human T1D and carry important implications for targeting Tfh cells and/or B cells therapeutically.

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          Author and article information

          Journal
          Diabetes
          Diabetes
          American Diabetes Association
          1939-327X
          0012-1797
          February 2017
          : 66
          : 2
          Affiliations
          [1 ] Department of Clinical Microbiology, Institute of Clinical Medicine, University of Eastern Finland, Kuopio, Finland.
          [2 ] Department of Pediatrics, Turku University Hospital and University of Turku, Turku, Finland.
          [3 ] School of Medicine, University of Tampere and Fimlab Laboratories, Pirkanmaa Hospital District, Tampere, Finland.
          [4 ] Tampere Center for Child Health Research, Tampere University Hospital, Tampere, Finland.
          [5 ] Department of Medicine, Kuopio University Hospital, Kuopio, Finland.
          [6 ] Institute of Clinical Medicine, University of Eastern Finland, Kuopio, Finland.
          [7 ] Institute of Public Health and Clinical Nutrition, University of Eastern Finland and Clinical Nutrition and Obesity Center, Kuopio University Hospital, Kuopio, Finland.
          [8 ] Department of Pediatrics, Medical Research Center, PEDEGO Research Unit, Oulu University Hospital and University of Oulu, Oulu, Finland.
          [9 ] Department of Physiology, Institute of Biomedicine, University of Turku, and Department of Pediatrics, Turku University Hospital, Turku, Finland.
          [10 ] Children's Hospital, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
          [11 ] Diabetes and Obesity Research Program, Research Programs Unit, University of Helsinki, Helsinki, Finland.
          [12 ] Folkhälsan Research Centre, Helsinki, Finland.
          [13 ] Immunogenetics Laboratory, University of Turku, Turku, Finland.
          [14 ] Department of Clinical Microbiology, Institute of Clinical Medicine, University of Eastern Finland, Kuopio, Finland tuure.kinnunen@uef.fi.
          Article
          db16-0714
          10.2337/db16-0714
          28108610

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