| First Author | Seo S | Year | 2001 |
| Journal | J Immunol | Volume | 166 |
| Issue | 6 | Pages | 3710-6 |
| PubMed ID | 11238611 | Mgi Jnum | J:67891 |
| Mgi Id | MGI:1931664 | Doi | 10.4049/jimmunol.166.6.3710 |
| Citation | Seo Sj, et al. (2001) Novel roles for lyn in b cell migration and lipopolysaccharide responsiveness revealed using anti-double-stranded dna ig transgenic mice. J Immunol 166(6):3710-6 |
| abstractText | Lyn-deficient mice produce Abs against dsDNA, yet exhibit exaggerated tolerance to the model Ag hen-egg lysozyme. To investigate this apparent contradiction, and to further examine the function of Lyn in Ag-engaged cells, we have used an anti-dsDNA Ig transgenic model. Previously, looking at these anti-dsDNA B cells in Lyn-sufficient BALB/c mice, we showed that they are regulated by functional inactivation (anergy). In the absence of Lyn, these anti-dsDNA B cells remain unable to secrete Ab. This suggests that functional inactivation of anti-dsDNA B cells does not depend on Lyn, and that the anti-dsDNA Abs that are produced in lyn(-/-) mice arise from a defect in another mechanism of B cell tolerance. Although the anti-dsDNA B cells remain anergic, Lyn deficiency does restore their ability to proliferate to LPS. This reveals a novel role for Lyn in mediating the LPS unresponsiveness that normally follows surface Ig engagement. Furthermore, Lyn deficiency leads to an altered splenic localization and EBV-induced molecule 1 ligand chemokine responsiveness of anti-dsDNA B cells, as well as an absence of marginal zone B cells, suggesting additional roles for Lyn in controlling the migration and development of specific B cell populations. |
