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A novel function of B lymphocytes from normal mice to suppress autoimmunity in (NZB × NZW)F 1 mice
Author(s) -
Ono S.,
Shao D.Z.,
Yamada S.,
Yang Y.,
Yamashita M.,
Hamaoka T.
Publication year - 2000
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2000.00005.x
Subject(s) - autoantibody , autoimmunity , b cell , immunology , antibody , biology , autoimmune disease , lipopolysaccharide , immunoglobulin m , immune system , endocrinology , medicine , immunoglobulin g
Summary In systemic autoimmune‐prone (NZB × NZW)F 1 (NZB/W F 1 ) mice, B‐cell abnormalities characterized by hypergammaglobulinaemia accompanying autoantibodies have been thought to be a main cause of the disease. To examine a possible regulatory role of B cells in the disease manifestations, we injected, intravenously (i.v.), normal or autoimmune B cells into non‐irradiated NZB/W F 1 mice. The injection of splenic B cells from major histocompatibility (MHC)‐matched or allogeneic normal mice caused a marked decrease in serum immunoglobulin G (IgG) levels of autoantibodies, delayed the appearance of proteinuria and prolonged life span, whereas treatment with splenic B cells from NZB/W F 1 or X‐linked immunodeficient (Xid) mice failed to suppress the autoimmunity. Moreover, in vitro polyclonal antibody responses to lipopolysaccharide (LPS) of NZB/W F 1 ‐derived B cells from the treated mice were markedly reduced. Interestingly, the treatment of NZB/W F 1 mice at 16, 18 and 20 or at 20, 22 and 24 weeks of age was more effective than that at 6, 8 and 10 weeks. The treatment also inhibited the development of surface IgG + (sIgG + ) B cells and splenomegaly, prominent in aged NZB/W F 1 mice. In addition, when untreated NZB/W F 1 responding B cells were precultured with normal B cells in vitro for 3 days, they also diminished the autoantibody production to subsequent LPS stimulation. Hence, the present results imply a novel function of normal B cells to ameliorate autoimmune disease in NZB/W F 1 mice by correcting their B‐cell abnormalities, and indicate that NZB/W F 1 and Xid mice possess defects in this regulatory B‐cell function.