| First Author | Mattsson N | Year | 2005 |
| Journal | Cell Immunol | Volume | 234 |
| Issue | 2 | Pages | 124-32 |
| PubMed ID | 16054613 | Mgi Jnum | J:100560 |
| Mgi Id | MGI:3588837 | Doi | 10.1016/j.cellimm.2005.06.005 |
| Citation | Mattsson N, et al. (2005) Expansion of CD22(lo) B cells in the spleen of autoimmune-prone flaky skin mice. Cell Immunol 234(2):124-32 |
| abstractText | Similar to murine models with compromised CD22/SHP-1 function, flaky skin (fsn) mutant mice exhibit lymphocyte hyperactivation and an autoimmune phenotype characterized by circulating autoantibodies to dsDNA and glomerulonephritis. Immunophenotyping of fsn/fsn splenic B cells was performed to determine if abnormalities in CD22 expression contributed to the phenotype. We identified an expansion of an IgM(bright) CD22(lo) population consistent with immature B-lymphocytes. While normal B-lymphocytes require IL-4 to achieve down-modulation of CD22 expression in response to BCR cross-linking, culture with anti-IgM alone led to reduced CD22 expression in fsn/fsn mice. Furthermore, when IL-4 was added to fsn/fsn cultures, no further reduction in CD22 expression was observed. This suggested that fsn/fsn B cells were pre-activated in vivo by chronic IL-4 exposure. A portion of these CD22(lo) cells expressed the B-1 surface marker CD11b. We contend that decreased activation thresholds among CD22(lo) B-lymphocytes contributes to the expansion of immature and B-1 B cell populations and to the development of autoimmune pathology in fsn/fsn mice. |
