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

Zheng Zhang1, Vasileios C Kyttaris, George C Tsokos

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

Journal of Immunology (Baltimore, Md. : 1950)
|August 7, 2009
PubMed

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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