Prevention of autoimmune symptoms in autoimmune-prone mice by elimination of B-1 cells |
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Authors: | Murakami Masao; Yoshioka Hideyuki; Shirai Toshikazu; Tsubata Takeshi; Honjo Tasuku |
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Institution: | 1 Departments of Medical Chemistry, Kyoto University Yoshida, Sakyo-ku, Kyoto 606, Japan
2 Geriatric Medicine, Faculty of Medicine, Kyoto University Yoshida, Sakyo-ku, Kyoto 606, Japan
3 Department of Pathology, Juntendo University School of Medicine 2-1-1 Hongo, Bunkyo-ku, Tokyo 113, Japan |
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Abstract: | Our recent studies on an autoantibody-transgenic mouse linedemonstrated that peritoneal B-1 cells are responsible for autoimmunesymptoms. However, whether B-1 cells in the peritoneum are generallyinvolved in the pathogenesis of autoimmune disease remains controversial.To test the possible involvement of peritoneal B-1 cells inautoimmune symptoms of autoimmune-prone NZB mice, we eliminatedthe peritoneal cells by hypotonic shock with repeated I.p. injectionof distilled water every 7 days into neonatal or 8-week-oldNZB mice. By this treatment, B-1 cells, which self- renew withinthe peritoneal cavity, are expected to be preferentially eliminated,while other peritoneal cells can be easily supplied from bonemarrows after this treatment indeed, in distilled water-treatedold NZB mice, the number of B-1 cells decreased in spleen aswell as in lamina propria of the gut but the numbers of conventionalB cells and T cells did not change. Moreover, the productionof autoantibodies against erythrocytes significantly decreasedand the occurrence of autoimmune hemolytic anemia was reducedin 12-month-old treated NZB mice. Similarly, the eliminationof peritoneal cells of NZB/NZW (NZB/W) F1; mice by water injectiondecreased anti-DNA IgG antibodies in the sera and reduced thepathological changes of the kidney. These results suggest thatperitoneal B-1 cells may be a source of autoantibody-producingcells in autoimmune diseases of NZB and NZB/W F1; mice. |
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Keywords: | autoimmunity B-1 |
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