| First Author | Hibbs ML | Year | 1995 |
| Journal | Cell | Volume | 83 |
| Issue | 2 | Pages | 301-11 |
| PubMed ID | 7585947 | Mgi Jnum | J:29356 |
| Mgi Id | MGI:76881 | Doi | 10.1016/0092-8674(95)90171-x |
| Citation | Hibbs ML, et al. (1995) Multiple defects in the immune system of Lyn-deficient mice, culminating in autoimmune disease. Cell 83(2):301-11 |
| abstractText | Mice homozygous for a disruption at the Lyn locus display abnormalities associated with the B lymphocyte lineage and in mast cell function. Despite reduced numbers of recirculating B lymphocytes, Lyn-/- mice are immunoglobulin M (IgM) hyperglobulinemic. Immune responses to T-independent and T-dependent antigens are affected. Lyn-/- mice fail to mediate an allergic response to IgE cross-linking, indicating that activation of LYN plays an indispensable role in Fc epsilon RI signaling. Lyn-/- mice have circulating autoreactive antibodies, and many show severe glomerulonephritis caused by the deposition of IgG immune complexes in the kidney, a pathology reminiscent of systemic lupus erythematosus. Collectively, these results implicate LYN as having an indispensable role in immunoglobulin-mediated signaling, particularly in establishing B cell tolerance. |
