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


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.

SUBMITTER: Khare SD 

PROVIDER: S-EPMC16246 | biostudies-literature | 2000 Mar

REPOSITORIES: biostudies-literature

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

Khare S D SD   Sarosi I I   Xia X Z XZ   McCabe S S   Miner K K   Solovyev I I   Hawkins N N   Kelley M M   Chang D D   Van G G   Ross L L   Delaney J J   Wang L L   Lacey D D   Boyle W J WJ   Hsu H H  

Proceedings of the National Academy of Sciences of the United States of America 20000301 7


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  ...[more]

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