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*
Cattedra di Immunologia, Dipartimento di Biologia e Patologia Cellulare e Molecolare, and
Dipartimento di Scienze Biomorfologiche, Universita di Napoli "Federico II," Napoli, Italy;
Laboratorio di Immunologia Cellulare, Azienda Ospedaliara "V. Monaldi," Napoli, Italy;
Centro di Endocrinologia e Oncologia Sperimentale-Consiglio Nazionale delle Ricerche (CEOS-CNR), Napoli, Italy; and
¶
Department of Immunology and
|| Endocrine Unit, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom
Recent evidence indicates that leptin modifies T cell immunity, and may provide a key link between nutritional deficiency and immune dysfunction. To study the influence of leptin on autoimmunity, susceptibility to experimental autoimmune encephalomyelitis induced by immunization with a myelin-derived peptide was examined in leptin-deficient, C57BL/6J-ob/ob mice, with or without leptin replacement, and in wild-type controls. Leptin replacement converted disease resistance to susceptibility in the C57BL/6J-ob/ob mice; this was accompanied by a switch from a Th2 to Th1 pattern of cytokine release and consequent reversal of Ig subclass production. Our findings suggest that leptin is required for the induction and maintenance of an effective proinflammatory immune response in the CNS.
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