Relatively Increased Number of Liver Foxp3~+ Regulatory T Cells against Hepatic Lesions in Murine Lupus

Systemic lupus erythematosus(SLE) is a multiple organ autoimmune disorder,including the liver,but the possible reason in impairment in the liver is still unclear.Our present study assessed alterations of transcription factor Foxp3+ regulatory T cells(Tregs) and several other immune molecules [progra...

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Published inJournal of Huazhong University of Science and Technology. Medical sciences Vol. 31; no. 4; pp. 476 - 481
Main Author 余立凯 黄安斌 王玮炜 杜戎 沈凌汛 侯晓华
Format Journal Article
LanguageEnglish
Published Heidelberg Huazhong University of Science and Technology 01.08.2011
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Summary:Systemic lupus erythematosus(SLE) is a multiple organ autoimmune disorder,including the liver,but the possible reason in impairment in the liver is still unclear.Our present study assessed alterations of transcription factor Foxp3+ regulatory T cells(Tregs) and several other immune molecules [programmed cell death 1 and its ligand(PD1 and PD-L1),and interleukin 10(IL-10) and transform growth factor β(TGF-β)] in the liver and other major organs of lupus-prone BXSB mice by flow cytometry,real-time quantitative reverse transcription PCR,and enzyme-linked immunosorbent assay.Results showed that both frequency and number of Foxp3+ Tregs were dramatically reduced in the thymus,spleen and kidney of the BXSB mice(P0.05),but those in the liver were kept in nearly normal range,when compared to negative control C57BL/6 mice.In comparison to control mice,the mRNA levels of Foxp3,PD1 and PD-L1 were significantly decreased in the kidneys of BXSB mice(P0.05),but there was no significant difference in the livers of the BXSB mice(P0.05).Protein levels of IL-10 and TGF-β in serum showed no significant difference between BXSB and C57BL/6 mice,but were significantly increased in the kidneys and livers of BXSB mice as compared with those in C57BL/6 mice(P0.05).These results suggest that reduced Foxp3+ Tregs are involved in the pathogenesis of SLE in BXSB mice,and relatively higher number of these cells in the livers than in the other target organs could constitute a protective mechanism against hepatic lesions in lupus-prone mice,which may provide insights into development of new therapeutic approaches in SLE patients.
Bibliography:Foxp3; hepatic lesion; lupus; BXSB mice
Systemic lupus erythematosus(SLE) is a multiple organ autoimmune disorder,including the liver,but the possible reason in impairment in the liver is still unclear.Our present study assessed alterations of transcription factor Foxp3+ regulatory T cells(Tregs) and several other immune molecules [programmed cell death 1 and its ligand(PD1 and PD-L1),and interleukin 10(IL-10) and transform growth factor β(TGF-β)] in the liver and other major organs of lupus-prone BXSB mice by flow cytometry,real-time quantitative reverse transcription PCR,and enzyme-linked immunosorbent assay.Results showed that both frequency and number of Foxp3+ Tregs were dramatically reduced in the thymus,spleen and kidney of the BXSB mice(P0.05),but those in the liver were kept in nearly normal range,when compared to negative control C57BL/6 mice.In comparison to control mice,the mRNA levels of Foxp3,PD1 and PD-L1 were significantly decreased in the kidneys of BXSB mice(P0.05),but there was no significant difference in the livers of the BXSB mice(P0.05).Protein levels of IL-10 and TGF-β in serum showed no significant difference between BXSB and C57BL/6 mice,but were significantly increased in the kidneys and livers of BXSB mice as compared with those in C57BL/6 mice(P0.05).These results suggest that reduced Foxp3+ Tregs are involved in the pathogenesis of SLE in BXSB mice,and relatively higher number of these cells in the livers than in the other target organs could constitute a protective mechanism against hepatic lesions in lupus-prone mice,which may provide insights into development of new therapeutic approaches in SLE patients.
Likai YU 1,Anbin HUANG 1,Weiwei WANG 1,Rong DU 1,Lingxun SHEN 1,Xiaohua HOU 2# 1Department of Rheumatology,2Department of Gastroenterology,Union Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430022,China
42-1679/R
ISSN:1672-0733
1993-1352
DOI:10.1007/s11596-011-0476-2