title: Identification and characterization of IL-2 hyper-responsive NZB/WF1 CD5- B cells.
abstract: The responsiveness of CD5- and CD5+ B cells of BALB/c and NZB/WF1 mice to various cytokines was examined with respect to their growth and differentiation. BALB/c splenic CD5- B cells required longer incubation with IL-2 or pretreatment with IL-4 to respond to IL-2 by DNA synthesis, whereas NZB/WF1 CD5- B cells were highly competent to IL-2. Flow cytometric analysis demonstrated that NZB/WF1 and BALB/c CD5- B cells had higher and intermediate proportions of B cells positive for IL-2R beta, respectively. On the other hand, BALB/c and NZB/WF1 splenic CD5+ B cells consisted of lower proportion of B cells positive for IL-2R beta than did their corresponding CD5- B cells and grew meagerly in response to IL-2. Peritoneal exudative CD5+ B cells of NZB/WF1 mice lacked IL-2R beta mRNA expression and failed to respond to IL-2. Although both BALB/c and NZB/WF1 CD5- B cells pretreated with anti-IgM, IL-4, and IL-5 responded to IL-2 by DNA synthesis, only BALB/c CD5- B cells developed into IgM-producing cells. Furthermore, BALB/c, but not NZB/WF1 CD5-, B cells pretreated with anti-IgM and IL-5 responded to IL-2 by IgM production without DNA synthesis. Thus, cross-talk between IL-4 and IL-2 operated in the growth responses of both BALB/c and NZB/WF1 splenic CD5- B cells, whereas cross-talk between IL-5 and IL-2 operated only in the differentiation of BALB/c CD5- B cells, providing us with another intriguing functional abnormality of NZB/WF1 B cells.
authors.affiliation: Third Department of Internal Medicine, Hyogo College of Medicine, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Hirose
authors.forename: K
authors.initials: K
authors.lastname: Nakanishi
authors.forename: T
authors.initials: T
authors.lastname: Yoshimoto
authors.forename: S
authors.initials: S
authors.lastname: Kashiwamura
authors.forename: K
authors.initials: K
authors.lastname: Hiroishi
authors.forename: H
authors.initials: H
authors.lastname: Matsumoto
authors.forename: T
authors.initials: T
authors.lastname: Hamaoka
authors.forename: S
authors.initials: S
authors.lastname: Shinka
authors.forename: K
authors.initials: K
authors.lastname: Higashino
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000032:analysis; D000954:Antigens, Surface / Q000032:analysis; D001327:Autoimmune Diseases / Q000276:immunology*; D016175:B-Lymphocyte Subsets / Q000276:immunology*; D018956:CD5 Antigens; D002454:Cell Differentiation / Q000187:drug effects; D002455:Cell Division / Q000187:drug effects; D016207:Cytokines / Q000494:pharmacology; D005260:Female; D000949:Histocompatibility Antigens Class II / Q000032:analysis; D007072:Immunoglobulin D / Q000378:metabolism; D007376:Interleukin-2 / Q000494:pharmacology*; D015847:Interleukin-4 / Q000494:pharmacology; D017493:Leukocyte Common Antigens; D008213:Lymphocyte Activation / Q000187:drug effects; D051379:Mice; D008807:Mice, Inbred BALB C; D008814:Mice, Inbred NZB / Q000276:immunology*; D017455:Receptors, IgE / Q000032:analysis; D015375:Receptors, Interleukin-2 / Q000502:physiology*
chemical_list: D015703:Antigens, CD; D000954:Antigens, Surface; D018956:CD5 Antigens; D016207:Cytokines; D000949:Histocompatibility Antigens Class II; D007072:Immunoglobulin D; D007376:Interleukin-2; D017455:Receptors, IgE; D015375:Receptors, Interleukin-2; D015847:Interleukin-4; D017493:Leukocyte Common Antigens