title: Relatively increased number of liver Foxp(3+) regulatory T cells against hepatic lesions in murine lupus.
abstract: 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 (P<0.05), 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 (P<0.05), but there was no significant difference in the livers of the BXSB mice (P>0.05). 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 (P<0.05). 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.
authors.affiliation: Department of Rheumatology, Huazhong University of Science and Technology, Wuhan, 430022, China.
authors.forename: Likai
authors.initials: L
authors.lastname: Yu
authors.affiliation: Department of Rheumatology, Huazhong University of Science and Technology, Wuhan, 430022, China.
authors.forename: Anbin
authors.initials: A
authors.lastname: Huang
authors.affiliation: Department of Rheumatology, Huazhong University of Science and Technology, Wuhan, 430022, China.
authors.forename: Weiwei
authors.initials: W
authors.lastname: Wang
authors.affiliation: Department of Rheumatology, Huazhong University of Science and Technology, Wuhan, 430022, China.
authors.forename: Rong
authors.initials: R
authors.lastname: Du
authors.affiliation: Department of Rheumatology, Huazhong University of Science and Technology, Wuhan, 430022, China.
authors.forename: Lingxun
authors.initials: L
authors.lastname: Shen
authors.affiliation: Department of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. houxh@public.wh.hb.cn.
authors.forename: Xiaohua
authors.initials: X
authors.lastname: Hou
mesh_terms: D000818:Animals; D051858:Forkhead Transcription Factors / Q000276:immunology*; D008099:Liver / Q000276:immunology*; D008180:Lupus Erythematosus, Systemic / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*
chemical_list: D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse