title: The in vivo expression of type B CD23 mRNA in B-chronic lymphocytic leukemic cells is associated with an abnormally low CD23 upregulation by IL-4: comparison with their normal cellular counterparts.
abstract: We recently reported that the sera of chronic lymphocytic leukemia (CLL) patients contained 3-500 times more soluble CD23 (or IgE-BF) than the sera of patients with other lymphoproliferative diseases or normal individuals and that their B cells (B-CLLs) overexpressed CD23 Ag. In the present report, we extended these studies and showed that CD5+ B cells from all CLL patients (n = 15) co-express CD23 Ag. We next identified two additional major differences between B-CLLs and normal adult B cells. First, in contrast to normal adult B cells which exclusively express type A CD23 mRNA, freshly isolated B-CLLs expressed both type B and type A CD23 mRNA. Second, although IL-4 is a potent inducer of type B CD23 mRNA on normal B cells, an optimal concentration of IL-4 infranormally upregulated CD23 on highly purified B-CLLs both at the protein and at the molecular levels. However, co-stimulation of CLL PBMC with phytohemagglutinin (PHA) and IL-4 strongly upregulated CD23 on B-CLLs, reconstituting the high level of CD23 expression observed in vivo. We next attempted to relate B-CLLs to the CD5+ B cell subpopulations present in peripheral blood mononuclear cells (PBMC, n = 3), cord blood mononuclear cells (CBMC, n = 6) and tonsillar lymphocytes (TONS, n = 3) by analysing their co-expression of CD20, CD5 and CD23 Ag and their phenotypic regulation by IL-4. Our results indicated that B-CLLs presented some features in common with the CD23+ umbilical cord blood B cells in as much as, like in B-CLLs; (i) all CD23+ cord blood cells co-expressed CD5 Ag, (ii) freshly isolated CBMC expressed both type A and type B CD23 mRNA, and finally (iii) these cells weakly re-expressed CD23 Ag upon IL-4 stimulation as compared to adult PBMC.
authors.affiliation: University of Montreal, Notre-Dame Hospital, Research Center, Quebec, Canada.
authors.forename: S
authors.initials: S
authors.lastname: Fournier
authors.forename: I D
authors.initials: ID
authors.lastname: Tran
authors.forename: U
authors.initials: U
authors.lastname: Suter
authors.forename: G
authors.initials: G
authors.lastname: Biron
authors.forename: G
authors.initials: G
authors.lastname: Delespesse
authors.forename: M
authors.initials: M
authors.lastname: Sarfati
mesh_terms: D000944:Antigens, Differentiation, B-Lymphocyte / Q000235:genetics*; D001402:B-Lymphocytes / Q000276:immunology / Q000502:physiology; D001483:Base Sequence; D005312:Fetal Blood / Q000166:cytology / Q000502:physiology; D015973:Gene Expression Regulation, Leukemic / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D015847:Interleukin-4 / Q000494:pharmacology / Q000502:physiology*; D015451:Leukemia, Lymphocytic, Chronic, B-Cell / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D008969:Molecular Sequence Data; D012333:RNA, Messenger / Q000235:genetics*; D011961:Receptors, Fc / Q000235:genetics*; D017455:Receptors, IgE; D015854:Up-Regulation / Q000187:drug effects / Q000502:physiology*
chemical_list: D000944:Antigens, Differentiation, B-Lymphocyte; D012333:RNA, Messenger; D011961:Receptors, Fc; D017455:Receptors, IgE; D015847:Interleukin-4