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 1
Serum leptin increase precedes the acute onset of chronic-progressive 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 immunization with MOG_35–55 peptide. Leptin-deficient mice are EAE resistant and do not lose weight after immunization, whereas wild-type controls are EAE susceptible and lose body weight. (b) Serum leptin (bars) increases before clinical onset of EAE only in wild-type controls and is undetectable 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 (P = 0.0005, r = 0.89) between the change in serum leptin before and after immunization with MOG_35–55 peptide (Δ indicates the increase in serum leptin) and the CDI, calculated as the sum of each daily clinical score of each single mouse (n = 10). A significant correlation was observed in wild-type control mice but not in leptin-deficient mice. One representative experiment out of two is shown. y, equation that defines this regression; R2, regression coefficient, R, correlation coefficient.