title: Prevention of autoimmune symptoms in autoimmune-prone mice by elimination of B-1 cells.
abstract: Our recent studies on an autoantibody-transgenic mouse line demonstrated that peritoneal B-1 cells are responsible for autoimmune symptoms. However, whether B-1 cells in the peritoneum are generally involved in the pathogenesis of autoimmune disease remains controversial. To test the possible involvement of peritoneal B-1 cells in autoimmune symptoms of autoimmune-prone NZB mice, we eliminated the peritoneal cells by hypotonic shock with repeated i.p. injection of distilled water every 7 days into neonatal or 8-week-old NZB mice. By this treatment, B-1 cells, which self-renew within the peritoneal cavity, are expected to be preferentially eliminated, while other peritoneal cells can be easily supplied from bone marrows after this treatment. Indeed, in distilled water-treated old NZB mice, the number of B-1 cells decreased in spleen as well as in lamina propria of the gut but the numbers of conventional B cells and T cells did not change. Moreover, the production of autoantibodies against erythrocytes significantly decreased and the occurrence of autoimmune hemolytic anemia was reduced in 12-month-old treated NZB mice. Similarly, the elimination of peritoneal cells of NZB/NZW (NZB/W) F1 mice by water injection decreased anti-DNA IgG antibodies in the sera and reduced the pathological changes of the kidney. These results suggest that peritoneal B-1 cells may be a source of autoantibody-producing cells in autoimmune diseases of NZB and NZB/W F1 mice.
authors.affiliation: Department of Medical Chemistry, Faculty of Medicine, Kyoto University, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Murakami
authors.forename: H
authors.initials: H
authors.lastname: Yoshioka
authors.forename: T
authors.initials: T
authors.lastname: Shirai
authors.forename: T
authors.initials: T
authors.lastname: Tsubata
authors.forename: T
authors.initials: T
authors.lastname: Honjo
mesh_terms: D000744:Anemia, Hemolytic, Autoimmune / Q000276:immunology / Q000517:prevention & control; D000818:Animals; D000974:Antibodies, Antinuclear / Q000096:biosynthesis / Q000276:immunology; D001327:Autoimmune Diseases / Q000276:immunology / Q000517:prevention & control*; D016175:B-Lymphocyte Subsets / Q000187:drug effects / Q000276:immunology*; D005260:Female; D007074:Immunoglobulin G / Q000096:biosynthesis; D007274:Injections, Intraperitoneal; D008181:Lupus Nephritis / Q000276:immunology / Q000517:prevention & control; D008212:Lymphocyte Depletion; D051379:Mice; D008807:Mice, Inbred BALB C; D008814:Mice, Inbred NZB; D014867:Water / Q000008:administration & dosage
chemical_list: D000974:Antibodies, Antinuclear; D007074:Immunoglobulin G; D014867:Water