Mice transgenic for BAFF develop lymphocytic disorders along with autoimmune manifestations.
Details
State: Public
Version: author
Serval ID
serval:BIB_DBCE91255287
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Mice transgenic for BAFF develop lymphocytic disorders along with autoimmune manifestations.
Journal
Journal of Experimental Medicine
ISSN
0022-1007 (Print)
ISSN-L
0022-1007
Publication state
Published
Issued date
1999
Volume
190
Number
11
Pages
1697-1710
Language
english
Abstract
The cause of many autoimmune and inflammatory diseases is unresolved, although dysregulated production of tumor necrosis factor (TNF) family members appears to be important in many cases. BAFF, a new member of the TNF family, binds to B cells and costimulates their growth in vitro. Mice transgenic for BAFF have vastly increased numbers of mature B and effector T cells, and develop autoimmune-like manifestations such as the presence of high levels of rheumatoid factors, circulating immune complexes, anti-DNA autoantibodies, and immunoglobulin deposition in the kidneys. This phenotype is reminiscent of certain human autoimmune disorders and suggests that dysregulation of BAFF expression may be a critical element in the chain of events leading to autoimmunity.
Keywords
Animals, Antibodies, Antinuclear/blood, Autoantibodies/blood, Autoimmune Diseases/genetics, Autoimmune Diseases/immunology, B-Cell Activating Factor, B-Lymphocytes/immunology, Flow Cytometry, Humans, Immunoglobulin A/blood, Immunoglobulin G/blood, Immunoglobulin M/blood, Immunoglobulins/metabolism, Kidney/immunology, Kidney/pathology, Kinetics, Leukocyte Count, Lung/immunology, Lymphatic Diseases/genetics, Lymphatic Diseases/immunology, Membrane Proteins/genetics, Membrane Proteins/immunology, Mice, Mice, Transgenic, Reverse Transcriptase Polymerase Chain Reaction, Rheumatoid Factor/blood, T-Lymphocytes/immunology, Tumor Necrosis Factor-alpha/genetics, Tumor Necrosis Factor-alpha/immunology
Pubmed
Web of science
Open Access
Yes
Create date
24/01/2008 16:18
Last modification date
20/08/2019 17:00