Abstract：
:NZB mice demonstrate common and consistent abnormalities in B-cell activation and signalling. One of the hallmark characteristics of lupus disease is the prevalent hypergammaglobulinaemia, composed primarily of anti-nuclear antibodies. In addition to the hyperproliferation seen in mice exhibiting disease, the B cells also demonstrate a marked degree of hyperactivity in response to B-cell receptor occupancy. This points to an intrinsic defect in the signalling pathways regulating the response to an activation event. Correspondingly, B cells of NZB mice exhibit a significant lack of phosphatase activity, both at baseline and in response to stimulation. This is directly reflected by a higher level of phosphorylation of tyrosine residues. Individually, SAPK and SHIP-1, both players in the B-cell receptor signalling cascade, are also found to be abnormally phosphorylated in the NZB mouse.
journal_name
J Autoimmunjournal_title
Journal of autoimmunityauthors
Tuscano JM,Hsu TC,McKnight H,Ansari AA,Gershwin MEdoi
10.1006/jaut.2002.0607subject
Has Abstractpub_date
2002-11-01 00:00:00pages
103-9issue
3eissn
0896-8411issn
1095-9157pii
S0896841102906074journal_volume
19pub_type
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更新日期：2016-11-01 00:00:00
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doi：10.1006/jaut.1994.1040
更新日期：1994-10-01 00:00:00
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