Table II.

Neurological impairment in leptin-deficient and wild-type control mice treated or not with rleptin and adoptively transferred with MOG35–55 peptide-specific wild-type T cellsa

MiceIncidenceOnset (range) (days)MortalityDuration (days)Clinical ScoreInitial Body Weight (g)Final Body Weight (g)
C57BL/6J-ob/ob PBS0/6 (0.0%)0.0 (0–0)0/6 (0.0%)0.00.050.7 ± 1.953.0 ± 0.7
C57BL/6J-ob/ob PBS-pair fed0/6 (0.0%)0.0 (0–0)0/6 (0.0%)0.00.051.5 ± 1.737.9 ± 0.5
C57BL/6J-ob/ob rleptin6/6 (100.0%)7.1 ± 1.8 (5–10)0/6 (0.0%)18.0b1.9 ± 0.5b50.4 ± 2.024.8 ± 1.2b
C57BL/6J PBS6/6 (100.0%)8.3 ± 2.0 (5–10)0/6 (0.0%)18.0c1.8 ± 0.4c21.2 ± 1.021.6 ± 2.0
C57BL/6J rleptin6/6 (100.0%)5.2 ± 0.9 (4–7)1/6 (16.7%)22.0d2.8 ± 0.4d21.5 ± 1.518.9 ± 0.8d
  • a Mice were adoptively transferred with 2.5 × 107 MOG35–55 peptide specific highly encephalitergic T cells obtained from draining lymph nodes and spleens of C57BL/6J wild-type donors, previously immunized with MOG35–55 peptide. Mice were observed daily for 30 days. Treatment with PBS or rleptin was performed starting 3 days before the adoptive transfer and continuing over a period of 25 days. None of the control mice (n = 5 for each group) adoptively transferred with PBS or T cells from unprimed animals and with pertussis toxin developed disease (data not shown). Data are cumulated and averaged from one experiment and they are presented as mean ± SD.

  • b p < 0.01 compared with C57BL/6J-ob/ob PBS and C57BL/6J-ob/ob PBS-pair fed.

  • c NS compared with C57BL/6J-ob/ob rleptin.

  • d p < 0.05 compared with C57BL/6J PBS.