T Cell Tolerance to Germline-Encoded Antibody Sequences in a Lupus-Prone Mouse

The BCR V region has been implicated as a potential avenue of T cell help for autoreactive B cells in systemic lupus erythematosus. In principle, either germline-encoded or somatically generated sequences could function as targets of such help. Preceding studies have indicated that class II MHC-rest...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2005-08, Vol.175 (4), p.2184-2190
Main Authors: Guo, Wenzhong, Smith, Diana, Guth, Amanda, Aviszus, Katja, Wysocki, Lawrence J
Format: Article
Language:English
Subjects:
Amino Acid Sequence
Animals
Antibody Diversity - genetics
Autoantibodies - biosynthesis
Autoantibodies - genetics
Chromatin - immunology
Clonal Anergy - genetics
Female
Genetic Predisposition to Disease
Germ-Line Mutation - genetics
Germ-Line Mutation - immunology
Hybridomas
Immunoglobulin Heavy Chains - administration & dosage
Immunoglobulin Heavy Chains - biosynthesis
Immunoglobulin Heavy Chains - genetics
Immunoglobulin Variable Region - administration & dosage
Immunoglobulin Variable Region - biosynthesis
Immunoglobulin Variable Region - genetics
Lupus Erythematosus, Systemic - genetics
Lupus Erythematosus, Systemic - immunology
Male
Mice
Mice, Inbred BALB C
Mice, Inbred NZB
Molecular Sequence Data
Somatic Hypermutation, Immunoglobulin
T-Lymphocyte Subsets - immunology
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Summary:The BCR V region has been implicated as a potential avenue of T cell help for autoreactive B cells in systemic lupus erythematosus. In principle, either germline-encoded or somatically generated sequences could function as targets of such help. Preceding studies have indicated that class II MHC-restricted T cells in normal mice attain a state tolerance to germline-encoded Ab diversity. In this study, we tested whether this tolerance is intact in systemic lupus erythematosus-prone (New Zealand Black x SWR)F1 mice (SNF1). Using a hybridoma sampling approach, we found that SNF1 T cells were tolerant to germline-encoded Ab sequences. Specifically, they were tolerant to germline-encoded sequences derived from a lupus anti-chromatin Ab that arose spontaneously in this strain. This was true both for diseased and prediseased mice. Thus, there does not appear to be a global defect in T cell tolerance to Ab V regions in this autoimmune-prone strain either before or during autoimmune disease.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.175.4.2184