Cellular and Molecular Mechanisms of Regulation of Autoantibody Production in Lupus

: The hyperactive interaction between helper T cells and autoimmune B cells in individuals predisposed to systemic lupus erythematosus (SLE) can be interrupted by induction of regulatory and suppressor T cells. Using two strategies—high dose tolerance to an immunoglobulin‐derived peptide, and minige...

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Bibliographic Details
Published in:Annals of the New York Academy of Sciences 2005-06, Vol.1051 (1), p.433-441
Main Authors: HAHN, BEVRA H., EBLING, FANNY, SINGH, RAM R., SINGH, RAM P., KARPOUZAS, GEORGE, LA CAVA, ANTONIO
Format: Article
Language:English
Subjects:
Antibodies, Antinuclear - biosynthesis
Autoantibodies - biosynthesis
CD8+ T cells
CD8-Positive T-Lymphocytes - physiology
Humans
Lupus Erythematosus, Systemic - immunology
regulatory T cells
suppressor T cells
systemic lupus erythematosus
T-Lymphocytes, Regulatory - physiology
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Summary:: The hyperactive interaction between helper T cells and autoimmune B cells in individuals predisposed to systemic lupus erythematosus (SLE) can be interrupted by induction of regulatory and suppressor T cells. Using two strategies—high dose tolerance to an immunoglobulin‐derived peptide, and minigene vaccination with DNA encoding T cell epitopes presented by MHC class I molecules—our group has induced at least three types of regulatory/suppressive T cells. They include CD8+ T cells that suppress helper T cells by cytokine secretion, CD8+ T suppressors that kill B cells making anti‐DNA antibodies, and peptide‐binding CD4+CD25+ regulatory T cells that suppress B cells by direct cell contact. Each of these lymphocyte subsets suppresses anti‐DNA antibody production and delays the onset of nephritis in BWF1 lupus‐prone mice. Patients with SLE have amino acid sequences similar to those from murine anti‐DNA antibodies used in these studies, and at similar locations in the VH regions of anti‐DNA immunoglobulins. Therefore, strategies described here might ultimately be useful in therapy of the human disease.
ISSN:0077-8923
1749-6632
DOI:10.1196/annals.1361.085