| First Author | Ochi H | Year | 1999 |
| Journal | Immunology | Volume | 98 |
| Issue | 4 | Pages | 595-603 |
| PubMed ID | 10594694 | Mgi Jnum | J:178285 |
| Mgi Id | MGI:5297794 | Doi | 10.1046/j.1365-2567.1999.00899.x |
| Citation | Ochi H, et al. (1999) Regulation of B-1 cell activation and its autoantibody production by Lyn kinase-regulated signallings. Immunology 98(4):595-603 |
| abstractText | The src-family protein tyrosine kinase, Lyn, has been reported to play a crucial role in the regulation of B-cell antigen receptor (BCR)-mediated signalling. To elucidate the role of Lyn in the maintenance of immunological tolerance and the prevention of B-1 cell activation and its autoantibody production, Lyn-deficient mice were crossed with transgenic mice carrying the immunoglobulin heavy and light chain genes encoding an autoantibody against mouse red blood cells. In the transgenic mice, most peripheral B cells expressed the B-1 cell phenotype. When the transgenic mice were bred in specific pathogen-free (SPF) conditions, B-1 cells were anergic and did not produce any autoantibody. In contrast, Lyn-deficient transgenic mice kept in the same SPF conditions revealed markedly increased numbers of activated B-1 cells and developed severe autoimmune haemolytic anaemia. Moreover, the mice had a huge splenomegaly containing a remarkable accumulation of erythroblasts, resulted from extramedullary erythropoiesis, in addition to the increased numbers of lymphoblast-like cells of the B-1 cell lineages. The present study demonstrates a crucial role of Lyn kinase in the regulation of B-1 cell activation and maintenance of tolerance. |
