MULTIPLE DEFECTS IN THE IMMUNE-SYSTEM OF LYN-DEFICIENT MICE, CULMINATING IN AUTOIMMUNE-DISEASE
- Author(s)
- Hibbs, ML; Tarlinton, DM; Armes, J; Grail, D; Hodgson, G; MAGLITTO, R; Stacker, SA; DUNN, ARR;
- Details
- Publication Year 1995-10-20,Volume 83,Issue #2,Page 301-311
- Journal Title
- CELL
- Publication Type
- Journal Article
- Abstract
- 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.
- Publisher
- CELL PRESS
- Keywords
- PROTEIN TYROSINE PHOSPHORYLATION; AFFINITY IGE RECEPTOR; CELL ANTIGEN RECEPTOR; LYMPHOCYTES-B; SRC FAMILY; KINASES; IMMUNOGLOBULIN; STIMULATION; ASSOCIATION; ALPHA
- Publisher's Version
- https://doi.org/10.1016/0092-8674(95)90171-X
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 1995-10-20 12:00:00