Phosphorylation abnormalities: NZB mice exhibit a B-cell signalling defect

Joseph Tuscano, Tom C. Hsu, Hayes McKnight, Aftab A. Ansari, M. Eric Gershwin

Research output: Contribution to journalArticle

6 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)103-109
Number of pages7
JournalJournal of Autoimmunity
Volume19
Issue number3
DOIs
StatePublished - Nov 2002

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Keywords

  • B cells
  • Murine lupus
  • Phosphorylation pathways

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

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