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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Multiple defects in the immune system of Lyn-deficient mice, culminating in autoimmune disease.

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.[1]

References

  1. Multiple defects in the immune system of Lyn-deficient mice, culminating in autoimmune disease. Hibbs, M.L., Tarlinton, D.M., Armes, J., Grail, D., Hodgson, G., Maglitto, R., Stacker, S.A., Dunn, A.R. Cell (1995) [Pubmed]
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