title: CD5+ B-cells at the onset of type I diabetes and in the prediabetic period.
abstract: OBJECTIVE
  B-cells expressing CD5 are associated with the production of autoantibodies and are present at increased levels in several autoimmune diseases. The aim of this study was to investigate the relationship of these cells to the development of type I diabetes and the presence of organ and non-organ-specific autoantibodies.
  
  
  METHODS
  We measured percentage levels of CD5+ B-cells in patients with recent-onset (n = 34) and long-standing (n = 21) type I diabetes and in a cohort of 18 identical twins of patients with type I diabetes studied prospectively, 8 of whom became diabetic (prediabetic twins) during the study; the rest remained nondiabetic after at least 7 years and are now unlikely to develop the disease. Forty-seven healthy individuals were studied as control subjects.
  
  
  RESULTS
  Percentage levels of total B-cells (CD20+) and the proportion expressing CD5 were increased in patients with recent-onset (P < 0.001 for both) but not long-standing type I diabetes compared with control subjects. Percentage levels of CD20+ B-cells were increased in prediabetic twins throughout the prediabetic period (P < 0.05), and there was an increased proportion of CD5-expressing B-cells that failed to reach statistical significance (P = 0.08). Percentage levels of CD20+ B-cells and the proportion expressing CD5 were normal throughout the study in twins remaining nondiabetic. No relationship between percentage levels of CD5+ B-cells and islet cell antibody, thyroid autoantibodies, or non-organ-specific autoantibodies was found.
  
  
  CONCLUSIONS
  These results show an increase in B-cell percentage levels at the diagnosis of type I diabetes, which is because of an expansion of the CD5+ subset. These changes are also evident in twins throughout the prediabetic period, which suggests that they are related to the processes that lead to diabetes.
authors.affiliation: Department of Immunology, King's College School of Medicine, London, U.K.
authors.forename: R A
authors.initials: RA
authors.lastname: Smerdon
authors.forename: M
authors.initials: M
authors.lastname: Peakman
authors.forename: M J
authors.initials: MJ
authors.lastname: Hussain
authors.forename: F S
authors.initials: FS
authors.lastname: Wong
authors.forename: P J
authors.initials: PJ
authors.lastname: Watkins
authors.forename: R D
authors.initials: RD
authors.lastname: Leslie
authors.forename: D
authors.initials: D
authors.lastname: Vergani
mesh_terms: D000328:Adult; D017668:Age of Onset; D015703:Antigens, CD / Q000097:blood*; D018951:Antigens, CD20; D000944:Antigens, Differentiation, B-Lymphocyte / Q000097:blood; D001323:Autoantibodies / Q000097:blood; D016175:B-Lymphocyte Subsets / Q000276:immunology*; D018956:CD5 Antigens; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000276:immunology*; D004200:Diseases in Twins; D005260:Female; D006801:Humans; D016130:Immunophenotyping; D008297:Male; D011236:Prediabetic State / Q000097:blood / Q000276:immunology*; D014430:Twins, Monozygotic
chemical_list: D015703:Antigens, CD; D018951:Antigens, CD20; D000944:Antigens, Differentiation, B-Lymphocyte; D001323:Autoantibodies; D018956:CD5 Antigens