
Identification of human cytomegalovirus phosphoprotein 65 in C57BL/6 and BXSB mice as a potential trigger of systemic lupus erythematosus related serum markers
Author(s) -
Yuan Zhang,
Tingting Jia,
Yang Pan,
Wenli Li,
Yu Sun,
Jinming Li,
Lunan Wang
Publication year - 2015
Publication title -
asian pacific journal of tropical biomedicine/asian pacific journal of tropical biomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.507
H-Index - 61
eISSN - 2588-9222
pISSN - 2221-1691
DOI - 10.1016/s2221-1691(15)30158-1
Subject(s) - phosphoprotein , immunology , medicine , identification (biology) , cytomegalovirus , lupus erythematosus , human cytomegalovirus , virology , virus , biology , viral disease , herpesviridae , phosphorylation , antibody , biochemistry , botany
Objective:To investigate the potential role of human cytomegalovirus lower matrix phosphoprotein 65 (HCMV-pp65) in murine systemic lupus erythematosus (SLE).Methods:The prokaryotic plasmid pET-28b-pp65 was constructed to express the HCMV-pp65 protein. BXSB mice and C57BL/6 mice were inoculated with pp65 eukaryotic plasmid pcDNA3.0-pp65 intramuscularly 5 times at 2-week intervals, and then the blood of the mice was subsequently collected via the retro-orbital vein. Indirect ELISAs were used to evaluate the concentration of anti-pp65 immunoglobulin G, anti-double-stranded DNA and antinuclear antibodies. Interleukin-1β and tumor necrosis factor-α were also determined by competitive ELISA. At the same time, 3 major SLE-related circulating microRNAs were examined by quantitative RT-PCR.Results:The early production of autoantibodies was observed in pp65-immunized male BXSB as well as C57BL/6 mice. Overexpression of interleukin-1β and tumor necrosis factor-α were detected in pp65-immunized male BXSB mice. Quantitative RT-PCR analyses showed that three SLE related microRNAs (microRNA-126, microRNA-125a, and microRNA-146a) were down-regulated in peripheral blood mononuclear cells of pp65-immunized mice.Conclusions:Our findings indicate that HCMV-pp65 immunization strongly triggers the development and progression of SLE-like disease in both BXSB and C57BL/6 mice, which indicates that the immune responses induced by HCMV-pp65 may be involved in the development of SLE