摘要
Lupus nephritis is the most common visceral complication in the patients with systemic lupus erythematosus （SLE）.It was evident that the anti-dsDNA antibodies were closely related to lupus nephritis, as seen in patients who had higher titers of serum anti-dsDNA antibodies had more severe renal lesions and even worse prognosis. So far it is still unknown how the dsDNA or anti-dsDNA antibody plays a role in the pathogenesis of lupus nephritis. The Trypanosoma equiperdum （TE） has uniformed dsDNA, no histone is found in both the cell nucleus and kinetonucleus. For this reason, TE became an optimal substrate used for detecting anti-dsDNA antibodies in SLE patients. It is proved that TE substrate is highly sensitive and specific. This reminds us to concern whether TE dsDNA share same SLE antigenic determinants with the pathogenic dsDNA in patients. Compared to the mammalian dsDNA, the kinetoplast DNA （kDNA） of TE has simpler molecular structure which makes it easier for purification. It offers us the possibility to establish lupus-like nephritis model by TE kDNA. We subcutaneously injected TE kDNA into normal mice. The result indicated lupus-like nephritis has been successfully induced by this simple and convenient protocol, which is useful to elucidate the particular role of dsDNA or anti-dsDNA antibody in lupus nephritis.
Lupus nephritis is the most common visceral complication in the patients with systemic lupus erythematosus （SLE）.It was evident that the anti-dsDNA antibodies were closely related to lupus nephritis, as seen in patients who had higher titers of serum anti-dsDNA antibodies had more severe renal lesions and even worse prognosis. So far it is still unknown how the dsDNA or anti-dsDNA antibody plays a role in the pathogenesis of lupus nephritis. The Trypanosoma equiperdum （TE） has uniformed dsDNA, no histone is found in both the cell nucleus and kinetonucleus. For this reason, TE became an optimal substrate used for detecting anti-dsDNA antibodies in SLE patients. It is proved that TE substrate is highly sensitive and specific. This reminds us to concern whether TE dsDNA share same SLE antigenic determinants with the pathogenic dsDNA in patients. Compared to the mammalian dsDNA, the kinetoplast DNA （kDNA） of TE has simpler molecular structure which makes it easier for purification. It offers us the possibility to establish lupus-like nephritis model by TE kDNA. We subcutaneously injected TE kDNA into normal mice. The result indicated lupus-like nephritis has been successfully induced by this simple and convenient protocol, which is useful to elucidate the particular role of dsDNA or anti-dsDNA antibody in lupus nephritis.
