Severe B Cell Hyperplasia and Autoimmune Disease in TALL-1 Transgenic Mice

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 β -actin promoter. The TALL-1 t...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 2000-03, Vol.97 (7), p.3370-3375
Main Authors: Khare, Sanjay D., Sarosi, Ildiko, Xia, Xing-Zhong, McCabe, Susan, Miner, Kent, Solovyev, Irina, Hawkins, Nessa, Kelley, Michael, Chang, David, Van, Gwyneth, Ross, Larry, Delaney, John, Wang, Ling, Lacey, David, Boyle, William J., Hsu, Hailing
Format: Article
Language:English
Subjects:
Animals
Antibodies
Antigen-Antibody Complex - analysis
Autoantibodies
Autoantibodies - immunology
Autoimmune diseases
Autoimmune Diseases - immunology
Autoimmune Diseases - pathology
B lymphocytes
B-Cell Activating Factor
B-Lymphocytes - immunology
B-Lymphocytes - pathology
Base Sequence
Biological Sciences
Cytokines
Disease
DNA Primers
Genetics
Hypergammaglobulinemia - immunology
Immunology
Kidney - immunology
Lupus
Membrane Proteins - genetics
Mice
Mice, Transgenic
Receptors
Rodents
Spleen
T lymphocytes
Transgenic animals
Tumor Necrosis Factor-alpha - genetics
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Summary: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 β -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.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.97.7.3370