title: Double-positive CD21+CD27+ B cells are highly proliferating memory cells and their distribution differs in mucosal and peripheral tissues.
abstract: BACKGROUND
  Several B-cell defects arise in HIV infected patients, particularly in patients with chronic infection and high viral load. Loss of memory B cells (CD27(+) B cells) in peripheral blood and lymphoid tissues is one of the major B cell dysfunctions in HIV and simian immunodeficiency virus (SIV) infection. Despite several studies, definitive identification of memory B cells based on CD27 surface expression has not been described. Similarly, the rates of cell turnover in different B cell subpopulation from lymphoid and mucosal tissues have not been well documented. In this study, we demonstrate the presence of memory B cell populations and define their distribution, frequency and immunophenotype with regards to activation, proliferation, maturation, and antibody production in normal rhesus macaques from different lymphoid tissues.
  
  
  RESULTS
  Thirteen healthy, uninfected rhesus macaques were selected for this study. CD20(+) B cells were isolated from peripheral blood and sorted based on CD27 and CD21 surface markers to define memory B cell population. All the B cell subpopulation was further characterized phenotypically and their cell turnover rates were evaluated in vivo following bromodeoxyuridine (BrdU) inoculation. Double positive (DP) CD21(+)CD27(+) B cells in both peripheral and lymphoid tissues are memory B cells, able to produce antibody by polyclonal activation, and without T cell help. Peripheral and lymphoid DP CD21(+)CD27(+) B cells were also able to become activated and proliferate at higher rates than other B cell subpopulations. Increased turnover of tonsillar memory B cells were identified compared to other tissues examined.
  
  
  CONCLUSIONS
  We suggest that this DP memory B cells play a major role in the immune system and their function and proliferation might have an important role in HIV/SIV mediated B cell dysregulation and pathogenesis.
authors.affiliation: Division of Microbiology, Tulane National Primate Research Center, Tulane University School of Medicine, Covington, Louisiana, United States of America.
authors.forename: Arpita
authors.initials: A
authors.lastname: Das
authors.forename: Huanbin
authors.initials: H
authors.lastname: Xu
authors.forename: Xiaolei
authors.initials: X
authors.lastname: Wang
authors.forename: Canddy L
authors.initials: CL
authors.lastname: Yau
authors.forename: Ronald S
authors.initials: RS
authors.lastname: Veazey
authors.forename: Bapi
authors.initials: B
authors.lastname: Pahar
mesh_terms: D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology* / Q000473:pathology; D049109:Cell Proliferation; D006678:HIV / Q000276:immunology; D015658:HIV Infections / Q000209:etiology / Q000276:immunology / Q000473:pathology; D000882:Haplorhini; D006801:Humans; D007156:Immunologic Memory; D009092:Mucous Membrane / Q000276:immunology; D017464:Receptors, Complement 3d / Q000032:analysis; D016097:Simian Acquired Immunodeficiency Syndrome / Q000209:etiology / Q000276:immunology / Q000473:pathology; D015302:Simian Immunodeficiency Virus / Q000276:immunology; D014018:Tissue Distribution; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7 / Q000032:analysis
chemical_list: D017464:Receptors, Complement 3d; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7