The adipocytokine leptin is associated with nutritional satiety, yet it also influences immune responses, as both leptin-deficient (ob/ob) mice and leptin receptor–deficient (db/db) mice are less prone to develop autoimmunity. In the Journal of Immunology, Procaccini et al. show that leptin signaling affects the axis of Akt and the nutrient sensor mTor in effector T cells. Leptin induces an autocrine feedback loop to activate PI(3)K-Akt-mTor, which leads to higher expression of leptin and its receptor. Inhibition of leptin signaling, even after ligation of T cell antigen receptor, diminishes the proliferation of effector T cells and IL-2 production. Conversely, leptin can partially restore T cell responsiveness in the presence of the inhibitor rapamycin. These findings confirm that nutritional status, as signaled via leptin production, directly intersects with the activation of effector T cells via the mTor pathway.

J. Immunol. (17 August 2012) doi:10.4049/jimmunol.120093