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Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 476-481, 2011.
Artigo em Chinês | WPRIM | ID: wpr-298590

RESUMO

Systemic lupus erythematosus (SLE) is a multiple organ autoimmune disorder,including theliver,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 trinscription 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.

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