title: In-depth characterization of CD24(high)CD38(high) transitional human B cells reveals different regulatory profiles.
abstract: CD24(high)CD38(high) transitional B cells represent cells at a key stage in their developmental pathway. In addition, these B cells have been widely ascribed regulatory functions and involvement in the control of chronic inflammatory diseases. However, the phenotypic and functional overlap between these cells and regulatory B cells remains controversial.
  
  
  
  In this study we wanted to explore the regulatory properties of CD24(high)CD38(high) human B cells.
  
  
  
  We used multicolor flow cytometry in combination with bioinformatics and functional studies to show that CD24(high)CD38(high) B cells can be distinguished into multiple subsets with different regulatory functions.
  
  
  
  For the first time, the study reveals that human transitional B cells encompass not only transitional type 1 and type 2 B cells, as previously suggested, but also distinct anergic type 3 B cells, as well as IL-10-producing CD27(+) transitional B cells. Interestingly, the latter 2 subsets differentially regulate CD4(+) T-cell proliferation and polarization toward TH1 effector cells. Additional analyses reveal that the percentage of type 3 B cells is reduced and the frequency of CD27(+) transitional B cells is increased in patients with autoimmune diseases compared with those in matched healthy subjects.
  
  
  
  This study provides evidence for the existence of different transitional B-cell subsets, each displaying unique phenotypic and regulatory functional profiles. Furthermore, the study indicates that altered distribution of transitional B-cell subsets highlights different regulatory defects in patients with different autoimmune diseases.
authors.affiliation: EA2216, INSERM ESPRI, ERI29, Université de Brest, and LabEx IGO, Brest, France.
authors.forename: Quentin
authors.initials: Q
authors.lastname: Simon
authors.affiliation: EA2216, INSERM ESPRI, ERI29, Université de Brest, and LabEx IGO, Brest, France.
authors.forename: Jacques-Olivier
authors.initials: JO
authors.lastname: Pers
authors.affiliation: EA2216, INSERM ESPRI, ERI29, Université de Brest, and LabEx IGO, Brest, France; Rheumatology Department, CHRU Brest Morvan, Brest, France.
authors.forename: Divi
authors.initials: D
authors.lastname: Cornec
authors.affiliation: EA2216, INSERM ESPRI, ERI29, Université de Brest, and LabEx IGO, Brest, France.
authors.forename: Laëtitia
authors.initials: L
authors.lastname: Le Pottier
authors.affiliation: William Harvey Research Institute, Queen Mary University of London, London, United Kingdom.
authors.forename: Rizgar A
authors.initials: RA
authors.lastname: Mageed
authors.affiliation: EA2216, INSERM ESPRI, ERI29, Université de Brest, and LabEx IGO, Brest, France. Electronic address: sophie.hillion@univ-brest.fr.
authors.forename: Sophie
authors.initials: S
authors.lastname: Hillion
mesh_terms: D051997:ADP-ribosyl Cyclase 1 / Q000276:immunology; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001172:Arthritis, Rheumatoid / Q000276:immunology; D051927:CD24 Antigen / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D005260:Female; D006084:Graft Rejection / Q000276:immunology; D015658:HIV Infections / Q000276:immunology; D006801:Humans; D016030:Kidney Transplantation; D008180:Lupus Erythematosus, Systemic / Q000276:immunology; D008297:Male; D008562:Membrane Glycoproteins / Q000276:immunology; D008875:Middle Aged; D054448:Precursor Cells, B-Lymphoid / Q000276:immunology*; D012859:Sjogren's Syndrome / Q000276:immunology
chemical_list: D051927:CD24 Antigen; C497889:CD24 protein, human; D016207:Cytokines; D008562:Membrane Glycoproteins; C498154:CD38 protein, human; D051997:ADP-ribosyl Cyclase 1
keywords: Transitional B cells; autoimmunity; chronic inflammatory diseases; immune regulation