title: Age-associated increase of CD5+ B cells in the liver of autoimmune (NZB x NZW) F1 mice.
abstract: The liver has been demonstrated to be a major site for extrathymic differentiation of T cells. In this study, an identification of CD5+ B cells, which are responsible for the onset of autoimmune disease by virtue of autoantibody production, was performed in autoimmune (NZB x NZW) F1 mice. An age-associated increase of CD5+ B cells was demonstrated in the liver of these mice. Although CD5+ B cells (i.e., CD5+IgM+ and CD5+B220+) constituted a minor population of hepatic mononuclear cells (MNC) (< 5%) when mice were young (8 weeks), a large population of CD5+ B cells (10 to 30% of whole MNC) was identified in the liver of mice aged 25 to 30 weeks after the onset of disease. Such age-dependent increase of CD5+ B cells was not observed in any other strains including NZB, NZW, C3H/He and BALB/c mice. The phenotype of hepatic CD5+ B cells was the same as that of CD5+ B cells in the peritoneal cavity and spleen, showing dull-CD5, bright-IgM and dull-B220. High levels of CD5+ B cells were observed in the peritoneal cavity and liver, but not in the spleen nor in any other lymphoid organs in mice aged 30 weeks. Radioimmunoassay of autoantibodies in the 5-day culture supernatants demonstrated that hepatic MNC were unable to produce any amounts of IgM- and IgG-autoantibodies against double-stranded DNA and single-stranded DNA, despite the increased proportion of CD5+ B cells. On the other hand, peritoneal exudate cells produced only IgM-, but not IgG-, autoantibodies, whereas splenic cells were able to produce both IgM- and IgG-autoantibodies.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Microbiology, Tohoku University School of Dentistry, Miyagi, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Ohteki
authors.forename: T
authors.initials: T
authors.lastname: Abo
authors.forename: A
authors.initials: A
authors.lastname: Kusumi
authors.forename: T
authors.initials: T
authors.lastname: Sasaki
authors.forename: S
authors.initials: S
authors.lastname: Shibata
authors.forename: S
authors.initials: S
authors.lastname: Seki
authors.forename: K
authors.initials: K
authors.lastname: Kumagai
mesh_terms: D000375:Aging / Q000276:immunology*; D000818:Animals; D015703:Antigens, CD / Q000096:biosynthesis*; D001323:Autoantibodies / Q000096:biosynthesis; D001402:B-Lymphocytes / Q000276:immunology*; D018956:CD5 Antigens; D004247:DNA / Q000276:immunology; D004277:DNA, Single-Stranded / Q000276:immunology; D005260:Female; D007136:Immunoglobulins / Q000096:biosynthesis; D016130:Immunophenotyping; D008099:Liver / Q000166:cytology / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D008814:Mice, Inbred NZB; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D015703:Antigens, CD; D001323:Autoantibodies; D018956:CD5 Antigens; D004277:DNA, Single-Stranded; D007136:Immunoglobulins; D004247:DNA