1. Upregulated BclG(L) expression enhances apoptosis of peripheral blood CD4+ T lymphocytes in patients with systemic lupus erythematosus.
- Author
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Luo N, Wu Y, Chen Y, Yang Z, Guo S, Fei L, Zhou D, Yang C, Wu S, Ni B, Hao F, and Wu Y
- Subjects
- Adult, Antibodies, Antinuclear blood, Antibodies, Antinuclear immunology, CD4-Positive T-Lymphocytes metabolism, CD4-Positive T-Lymphocytes pathology, Down-Regulation genetics, Down-Regulation immunology, Female, Gene Expression immunology, Gene Expression Profiling, Humans, Lupus Erythematosus, Systemic metabolism, Lupus Erythematosus, Systemic pathology, Lymphocyte Subsets metabolism, Lymphocyte Subsets pathology, Middle Aged, Oligonucleotide Array Sequence Analysis, Proteinuria urine, Proto-Oncogene Proteins c-bcl-2 genetics, RNA, Small Interfering genetics, Serum immunology, Transfection, Up-Regulation genetics, Apoptosis immunology, CD4-Positive T-Lymphocytes immunology, Lupus Erythematosus, Systemic immunology, Proto-Oncogene Proteins c-bcl-2 metabolism, Up-Regulation immunology
- Abstract
Increased lymphocyte apoptosis has been suggested to contribute to the development of systemic lupus erythematosus (SLE), but the critical factors involved in the apoptotic pathways are still unknown. By long serial analysis of gene expression (LongSAGE) profiles and microarray analyses, a novel apoptosis-related gene BclG(L) expression was found significantly increased in peripheral blood CD4+ T cells of SLE patients, which was correlated with the enhanced CD4+ T cells apoptosis, anti-nuclear antibody (ANA) titer and proteinuria. In vitro, BclG(L) expression could be specially upregulated by SLE serum stimulation and positively correlated with induced CD4+ T cell apoptosis. Enforcing BclG(L) overexpression by lentivirus could directly enhance CD4+ T cell apoptosis, but these apoptosis-inducing effects could be partially inhibited by knockdown of BclG(L) expression. Collectively, these results indicate that increased BclG(L) expression may contribute to the aberrant CD4+ T cell apoptosis which causes an inappropriate immune response and impaired homeostasis in SLE.
- Published
- 2009
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