Expanded Double Negative T Cells in Patients with Systemic Lupus Erythematosus Produce IL-17 and Infiltrate the Kidneys

Double negative (DN) T cells are expanded in patients with systemic lupus erythematosus (SLE) and stimulate autoantibody production as efficiently as CD4(+) T cells. In this study, we demonstrate that DN T cells from patients with SLE produce significant amounts of IL-17 and IFN-gamma, and expand wh...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2008-12, Vol.181 (12), p.8761-8766
Main Authors: Crispin, Jose C, Oukka, Mohamed, Bayliss, George, Cohen, Robert A, Van Beek, Christine A, Stillman, Isaac E, Kyttaris, Vasileios C, Juang, Yuang-Taung, Tsokos, George C
Format: Article
Language:English
Subjects:
Adult
CD4-Positive T-Lymphocytes - immunology
CD4-Positive T-Lymphocytes - metabolism
CD4-Positive T-Lymphocytes - pathology
CD8-Positive T-Lymphocytes - immunology
CD8-Positive T-Lymphocytes - metabolism
CD8-Positive T-Lymphocytes - pathology
Cell Movement - immunology
Cell Proliferation
Cells, Cultured
Humans
Immunophenotyping
Inflammation Mediators - metabolism
Inflammation Mediators - physiology
Interleukin-17 - biosynthesis
Kidney - immunology
Kidney - pathology
Lupus Erythematosus, Systemic - immunology
Lupus Erythematosus, Systemic - metabolism
Lupus Erythematosus, Systemic - pathology
Middle Aged
T-Lymphocyte Subsets - immunology
T-Lymphocyte Subsets - metabolism
T-Lymphocyte Subsets - pathology
Up-Regulation - immunology
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Summary:Double negative (DN) T cells are expanded in patients with systemic lupus erythematosus (SLE) and stimulate autoantibody production as efficiently as CD4(+) T cells. In this study, we demonstrate that DN T cells from patients with SLE produce significant amounts of IL-17 and IFN-gamma, and expand when stimulated in vitro with an anti-CD3 Ab in the presence of accessory cells. Furthermore, IL-17(+) and DN T cells are found in kidney biopsies of patients with lupus nephritis. Our findings establish that DN T cells produce the inflammatory cytokines IL-17 and IFN-gamma, and suggest that they contribute to the pathogenesis of kidney damage in patients with SLE.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.181.12.8761