Lep

Nutritional deprivation suppresses immune function, and the discovery of the obese gene and its protein product, leptin, has provided crucial insights into the hypothalamic regulation of body weight. Leptin, an adipocyte-derived hormone, is directly proportional to fat mass but can decrease rapidly during fasting or increase due to inflammatory mediators. Despite the recognition that impaired T-cell immunity occurs in mice lacking leptin (ob/ob) or its receptor (db/db), the underlying mechanism has not been fully explained. Additionally, reduced leptin levels and impaired cell-mediated immunity are also associated with low body weight in humans, and malnutrition increases susceptibility to infectious diseases. This study reveals that leptin specifically influences T-lymphocyte responses, enhancing naive T-cell proliferation while suppressing memory T-cell activity. Leptin also promotes Th1 cytokine production while inhibiting Th2 cytokines. Administration of leptin to mice counteracted the immunosuppressive effects of acute starvation. These findings propose that leptin plays a vital role in linking nutritional status with cellular immune function, offering a molecular mechanism for the immune dysfunction observed during starvation