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Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3370-5.

Severe B cell hyperplasia and autoimmune disease in TALL-1 transgenic mice.

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  • 1Department, Pharmacology, Amgen, 1 Amgen Center Drive, Thousand Oaks, CA 91320-1799, USA.

Abstract

TALL-1/Blys/BAFF is a member of the tumor necrosis factor (TNF) ligand superfamily that is functionally involved in B cell proliferation. Here, we describe B cell hyperplasia and autoimmune lupus-like changes in transgenic mice expressing TALL-1 under the control of a beta-actin promoter. The TALL-1 transgenic mice showed severe enlargement of spleen, lymph nodes, and Peyer's patches because of an increased number of B220+ cells. The transgenic mice also had hypergammaglobulinemia contributed by elevations of serum IgM, IgG, IgA, and IgE. In addition, a phenotype similar to autoimmune lupus-like disease was also seen in TALL-1 transgenic mice, characterized by the presence of autoantibodies to nuclear antigens and immune complex deposits in the kidney. Prolonged survival and hyperactivity of transgenic B cells may contribute to the autoimmune lupus-like phenotype in these animals. Our studies further confirm TALL-1 as a stimulator of B cells that affect Ig production. Thus, TALL-1 may be a primary mediator in B cell-associated autoimmune diseases.

PMID:
10716715
[PubMed - indexed for MEDLINE]
PMCID:
PMC16246
Free PMC Article

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