Leptin-Deficient Mice Are Protected from Accelerated Nephrotoxic Nephritis

Ruth M. Tarzi, H. Terence Cook, Ian Jackson, Charles D. Pusey, Graham M. Lord

Research output: Contribution to journalArticlepeer-review


Leptin is an adipose tissue-derived hormone that signals nutritional status to the hypothalamus. Recent evidence indicates that leptin modifies proinflammatory immune responses and may provide a key link between nutritional deficiency and immune dysfunction. To study the influence of leptin deficiency on immune-mediated renal disease, susceptibility to accelerated nephrotoxic nephritis was examined in leptin-deficient C57BL/6-ob/ob mice and C57BL/6 wild-type controls. The model was induced with sheep anti-mouse glomerular basement membrane antibody injected to mice preimmunized against sheep IgG, and mice were sacrificed 8 days after induction of disease. The leptin-deficient ob/ob mice were strongly protected from glomerular crescent formation, macrophage infiltration, glomerular thrombosis, and albuminuria in this model. Our findings suggest that leptin is required for the induction and maintenance of immune-mediated glomerulonephritis, and that blockade of the leptin axis might provide an attractive therapeutic possibility in human autoimmune disease.
Original languageEnglish
Pages (from-to)385-390
Number of pages6
JournalThe American journal of pathology
Issue number2
Publication statusPublished - 1 Feb 2004


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