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J Immunol. 2009 Sep 1;183(5):3160-9. doi: 10.4049/jimmunol.0900385. Epub 2009 Aug 5.

The role of IL-23/IL-17 axis in lupus nephritis.

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  • 1Division of Rheumatology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.


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.

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