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. Obesity is associated with many human diseases, including autoimmune diseases, metabolic syndrome, and inflammation. Leptin is one of the most thoroughly investigated cell-signaling molecules secreted by the fat tissues and is typically elevated in patients diagnosed with lupus (systemic lupus erythematosus [SLE]), an autoimmune disease in which the body’s immune system attacks healthy tissues in many organs. Studies using leptin-deficient mice have also demonstrated that leptin is involved in modulating immune cells. However, transgenic leptin mice do not develop SLE-like symptoms, which is probably due to differences between the immune systems of humans and mice. We show that, consistent with the human data, our transgenic leptin pig model develops a number of pathophysiological changes with multiorgan injuries resembling SLE. Our work supports an association between leptin and SLE-like symptoms as observed in human patients and implies a crucial role for leptin in promoting the development of SLE.

Background: The Psoriasis Area and Severity Index (PASI) and the Dermatology Life Quality Index (DLQI) are important evaluation tools for assessing psoriasis severity and guiding treatment options. However, the scores of PASI and DLQI are often inconsistent. Objective: This study aimed to identify the factors affecting the consistency between PASI and DLQI. Methods: The retrospective study was based on 4125 patients. We collected the PASI, DLQI, demographic and clinical characteristics data. Results: DLQI has a weak correlation with PASI (r=0.37; P< 0.001). For the DLQI > 10 groups, DLQI has almost no correlation with PASI (r=0.16; P< 0.001). There are 43.60% of mild-to-moderate patients (PASI< 10) in the DLQI> 10 groups. Our adjusted model showed that foot (OR=2.109; 95% CI:1.581– 2.815) involvement led to the greatest impairment of QoL except for PASI≥ 10 (OR=5.547; 95% CI:3.477– 8.845). Furthermore, DLQI impairment was associated with female (OR=1.336; 95% CI:1.071– 1.667); the age of 20– 39 subgroup (OR=1.795; 95% CI:1.100– 2.930); psoriatic arthritis (OR=1.718; 95% CI:1.208– 2.443); higher income (OR = 1.408; 95% CI: 1.067– 1.858); family history of psoriasis (OR=1.460; 95% CI:1.131– 1.885). Moreover, the influence of exposed lesions (such as scalp; face; neck; nails; and hands) were positively associated with severely impaired QoL. Conclusion: Dermatologists should recognize the underestimated disease burden of psoriasis patients and actively identify and treat mild-to-moderate patients with high burden. In particular, the foot was a significant contributor to the burden.