title: IL-2 expands and maintains IgM plasmablasts from a CD5+ subset contained within the germinal centre cell-enriched (surface IgD-/CD39- buoyant) fraction of human tonsil.
abstract: IL-2 was found to promote the rapid growth of a minority population contained within the germinal centre (GC) cell-enriched (CD39- and/or IgD- buoyant) fraction of human tonsillar B lymphocytes. The cells emerging in response to IL-2 had a high mitotic index and morphologically resembled plasmablasts. Cultures could be maintained in the absence of feeder cells for up to 3 weeks in IL-2 and were characterized by large amounts of IgM in their supernatants: approximately 40% of the cells contained readily detectable cytoplasmic IgM by day 10 of culture. Negligible quantities of IgG and IgA were found. The target population for IL-2-driven expansion and IgM secretion was smIg+/CD38+ and was subject to suppression by anti-IgM antibody. While only 8% of cells within the GC cell-enriched fraction were CD5+ (compared with 15% of high density resting B cells), their removal led to an 83% reduction in the amount of IgM produced in response to IL-2, IL2 selectively expanded this minor CD5+ subset such that by day 6 of culture they comprised 57% of all viable cells. Cultures established with IL-2 showed increasing expression of cytoplasmic Bcl-2 and withdrawal of growth factor resulted in cell death via apoptosis. We discuss these results in relation to CD5+ B cells and their potential role in antibody responses to TD antigens.
authors.affiliation: Department of Immunology, Medical School, Birmingham, UK.
authors.forename: M J
authors.initials: MJ
authors.lastname: Holder
authors.forename: S D
authors.initials: SD
authors.lastname: Abbot
authors.forename: A E
authors.initials: AE
authors.lastname: Milner
authors.forename: C D
authors.initials: CD
authors.lastname: Gregory
authors.forename: M
authors.initials: M
authors.lastname: Casamayor
authors.forename: G D
authors.initials: GD
authors.lastname: Johnson
authors.forename: I C
authors.initials: IC
authors.lastname: MacLennan
authors.forename: J
authors.initials: J
authors.lastname: Gordon
mesh_terms: D000251:Adenosine Triphosphatases; D015703:Antigens, CD / Q000276:immunology*; D017209:Apoptosis; D001081:Apyrase; D016175:B-Lymphocyte Subsets / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology; D018956:CD5 Antigens; D002478:Cells, Cultured; D004247:DNA / Q000096:biosynthesis; D005854:Germ Cells / Q000166:cytology / Q000276:immunology; D006801:Humans; D007072:Immunoglobulin D / Q000276:immunology*; D007075:Immunoglobulin M / Q000276:immunology*; D007376:Interleukin-2 / Q000276:immunology*; D019394:Ki-67 Antigen; D008213:Lymphocyte Activation / Q000276:immunology; D009363:Neoplasm Proteins / Q000276:immunology; D009687:Nuclear Proteins / Q000276:immunology; D014066:Palatine Tonsil / Q000166:cytology / Q000276:immunology*; D011518:Proto-Oncogene Proteins / Q000276:immunology; D019253:Proto-Oncogene Proteins c-bcl-2
chemical_list: D015703:Antigens, CD; D018956:CD5 Antigens; D007072:Immunoglobulin D; D007075:Immunoglobulin M; D007376:Interleukin-2; D019394:Ki-67 Antigen; D009363:Neoplasm Proteins; D009687:Nuclear Proteins; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D004247:DNA; D000251:Adenosine Triphosphatases; D001081:Apyrase; C067869:CD39 antigen