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SCIENTIFIC PUBLICATIONS BY ALR FUNDED RESEARCHERS

Shared signaling networks that fire up in lupus B cells isolated from genetically distinct mouse models - Tianfu Wu and Chandra Mohan

August 1, 2007

SLE is a chronic, multisystem autoimmune disease associated with the production of a myriad of autoantibodies, primarily against nuclear antigens. Some of these antibodies may be responsible for tissue damage in this disease. An increasing body of data demonstrates that intrinsic hyperactivity of B cells might represent a key phenomenon in the development of lupus, both in mice and humans. However, the underlying molecular mechanisms have not been fully elucidated. Work in several laboratories has revealed that the genetic manipulation of several signaling axes can apparently precipitate lupus-like disease. For instance, forced hyperexpression of PI3K or the antiapoptotic molecule bc1-2 as well as haploinsufficiency of the tumor suppressor phosphatase and tensin homolog(PTEN) have been shown to cause lymphoproliferative lupus.

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Source: Alliance for Lupus Research
Funded Research

 

 


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