Leptin surge precedes onset of autoimmune encephalomyelitis and correlates with development of pathogenic T cell responses
J. Clin. Invest. Veronica Sanna, et al. 111:241 doi:10.1172/JCI16721 [Go to this article.]

Figure 4
Starvation at priming with the encephalitogenic peptide of SJL/J females reduces the clinical severity of EAE by inducing a Th2 cytokine switch, reversible by recombinant leptin administration. (a) Mean clinical score (bars) and body weight (curves) of SJL/J female mice starved for 48 hours (hatched bars and circles), ad libitum–fed controls (black bars and triangles), and leptin-treated female mice (gray bars and squares). Starvation delayed disease onset and reduced clinical score and body-weight loss during the acute phase of the disease. Leptin replacement during the 48-hour starvation reversed the starvation-induced blunting of the disease, so that the EAE course was similar to that observed in the ad libitum–fed group. (b) Proliferative response of lymph node–derived T cells against PLP_139–151 is impaired after 48 hours of starvation when compared with the control group. (c and d) Starvation for 48 hours reduced IFN-γ secretion but increased IL-4 production. (e) Addition of recombinant leptin to T-cell cultures is able to partially restore the capacity of T cells from starved mice to secrete IFN-γ. One representative experiment out of two is shown.