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 2
Serum leptin increase precedes acute onset of adoptively induced EAE and correlates with disease susceptibility, body-weight loss, and food-intake inhibition in EAE-susceptible C57BL/6J wild-type mice but not in EAE-resistant leptin-deficient C57BL/6J ob/ob mice. (a) Mean clinical score (bars) and body weight (curves) of C57BL/6J wild-type littermate controls (black bars and triangles) and leptin-deficient C57BL/6J ob/ob mice (white bars and circles) after adoptive transfer of 2.5 × 10⁷ MOG_35–55–specific CD4⁺ T cells. Leptin-deficient mice are EAE resistant and do not lose weight after adoptive transfer, whereas wild-type controls are EAE susceptible and lose body weight. (b) Serum leptin (bars) significantly increases before clinical onset of EAE in wild-type controls but increases very little in leptin-deficient mice; this increase correlates with food-intake inhibition, which is only present in wild-type animals. (c) Simple regression analysis showing a significant correlation (r = 0.97, P = 0.004) between the change in serum leptin before and after adoptive transfer of MOG_35–55–specific CD4⁺ T cells (Δ indicates the increase in serum leptin) and the CDI, calculated as the sum of each daily clinical score of each single mouse (n = 5). A significant correlation was observed in wild-type control mice but not in leptin-deficient mice. One representative experiment of two is shown.