期刊
JOURNAL OF IMMUNOLOGY
卷 183, 期 5, 页码 3160-3169出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0900385
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资金
- National Institute of Health [R01 A142269, R01 A149954, 1 K23 AR055672-01 A1]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI042269, R01AI049954] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [K23AR055672] Funding Source: NIH RePORTER
T cells that express IL-17 infiltrate the kidneys of patients with systemic lupus erythematosus. A significant proportion of these cells are CD3(+)CD4(-)CD8(-) double-negative T cells. In this study, we show that double-negative T cells from MRL/lpr mice express high amounts of IL-17 and that as disease progressively worsens, the expression of IL-17 and of IL-23 receptor in lymphocytes from these mice increases. Lymph node cells from lupus-prone mice, but not control mice, treated in vitro with IL-23 induce nephritis when transferred to non-autoimmune, lymphocyte-deficient Rag-1(-/-) mice. Kidney specimens from these recipient mice show significant Ig and complement deposition. The data indicate that an aberrantly active IL-23/IL-17 axis contributes to the development of nephritis in lupus-prone mice. The Journal of Immunology, 2009, 183: 3160-3169.
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