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LSO-005 Type I interferon affects Th22 cell differentiation participated in the pathogenesis of lupus nephritis
  1. Haojie Xu1,2,
  2. Rong Li1,2 and
  3. Lidan Zhao1
  1. 1Department of Rheumatology, Peking Union Medical College Hospital, China
  2. 2Graduate School, Chinese Academy of Medical Sciences and Peking Union Medical College, China


Background Lupus nephritis (LN) is one of the most common organ-specific injury of systemic lupus erythematosus (SLE) and has great influence on patients’ prognosis. Some research showed that interleukin (IL) -22 was enriched in the kidney tissue of MRL/lpr mice, and it was related to kidney lesions. The proportion of Th22 cells and IL-22 in periphery blood mononucleated cell (PBMC) and kidney tissue of LN patients were found increased, suggesting that IL-22/Th22 may be participated in the development of LN. About seventy-five percent of SLE patients showed significantly up-regulated of serum IFN-α (the main active component of IFN-I) and increased transcription of IFN-α-regulated genes in PBMC. Injected with IFN-α showed lupus phenotype increased in MRL/lpr mice.

Methods The effect of IFN-I on Th22 cell differentiation and the related key intracellular signaling pathway were investigated by in vitro cell experiments and in vivo animal model intervention, to explore whether IFN-I affects IL-22 production and Th22 differentiation.

Results Complement 3 levels were lower and SLEDAI-2K were higher in the LN group than in the non-LN group. Comparison of IL-22/IL-22R1 immunohistochemical (IHC) images in kidney between healthy control (HC) and LN patients, and the quantitative levels of IL-22/IL-22R1 in the LN group were quite higher than in the HC group. Similar results could be found in comparison between premortem (8 weeks) and postmortem (27 weeks) NZB/W F1 mice. Flow cytometry showed the high concentration of IFN-α could be inhibitor of the differentiation of Th22 cell.

Conclusions IL-22/Th22 could be participated in the development of LN, and IFN-I may play a significant role in activating the IL-22/Th22 pathway.

  • Type I interferon
  • Th22 cells
  • Lupus nephritis

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