Abstract
Leptin is a well-known adipokine that plays a critical role in immune responses. To further explore the immunological roles of leptin, we developed a transgenic leptin pig controlled by the pig leptin (pleptin) promoter to overexpress leptin. Symptoms typically associated with systemic lupus erythematosus (SLE) were evident in this transgenic pig strain, including anemia, leukopenia, and thrombocytopenia as well as kidney and liver impairment. Histologically, there were increased immunoglobulin G (IgG) levels, elevated antiplatelet antibody (APA) levels, and deposition of immune complexes in the kidney and liver. In addition, anti-double-stranded DNA antibodies (dsDNAs), antinuclear antibodies (ANAs), and antinucleosome antibodies (ANuAs) were all significantly increased in serum immunological examinations. These findings were also accompanied by repression of the regulatory T cell (Treg) ratio. Significantly, glucocorticoid experimental therapies partially relieved the autoimmune responses and bleeding symptoms observed in these transgenic leptin pigs. Together, these results indicate that leptin plays a critical role in the development of autoimmune disorders and demonstrate that our transgenic leptin pigs can act as a valuable model of SLE.
Highlights
Systemic lupus erythematosus (SLE) is a type of complex disease that can be caused by both genetic and environmental factors [1]
Leptin is one of the most thoroughly investigated cellsignaling molecules secreted by the fat tissues and is typically elevated in patients diagnosed with lupus, an autoimmune disease in which the body’s immune system attacks healthy tissues in many organs
Studies using leptindeficient mice have demonstrated that leptin is involved in modulating immune cells
Summary
Systemic lupus erythematosus (SLE) is a type of complex disease that can be caused by both genetic and environmental factors [1]. Multiple genomic loci have been reported to be associated with SLE [3,4,5,6,7], and various environmental factors, such as obesity, sunlight, infection, and exogenous estrogen, have been shown to contribute to its development [8]. SLE-like symptoms were not found in transgenic leptin mice, which is likely due to differences between the immune systems of humans and mice [10].
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