Leptin Modulates Allograft Survival by Favoring a Th2 and a Regulatory Immune Profile

Author(s):Show less -

Moraes-Vieira, P. M. M. ^[1] ; Bassi, E. J. ^[1] ; Larocca, R. A. ^{[2, 3, 4]} ; Castoldi, A. ^[1] ; Burghos, M. ^[1] ; Lepique, A. P. ^[1] ; Quintana, F. J. ^[5] ; Araujo, R. C. ^[6] ; Basso, A. S. ^[7] ; Strom, T. B. ^{[2, 3, 4]} ; Camara, N. O. S. ^{[8, 1]}

Affiliation

^[1] Univ Sao Paulo, Inst Biomed Sci, Dept Immunol, Sao Paulo - Brazil

^[2] Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02215 - USA

^[3] Harvard Univ, Sch Med, Boston, MA - USA

^[4] Transplant Inst, Boston, MA - USA

^[5] Harvard Univ, Brigham & Womens Hosp, Sch Med, Ctr Neurol Dis, Boston, MA 02115 - USA

^[6] Univ Fed Sao Paulo, Dept Biophys, Sao Paulo - Brazil

^[7] Univ Fed Sao Paulo, Dept Microbiol Immunol & Parasitol, Sao Paulo - Brazil

^[8] Univ Fed Sao Paulo, Div Nephrol, Sao Paulo - Brazil

• Document type: Journal article
• Source: AMERICAN JOURNAL OF TRANSPLANTATION; v. 13, n. 1, p. 36-44, JAN 2013.
• Web of Science Citations: 24

Abstract

Leptin, an adipose-secreted hormone, links metabolism and immunity. Our aim was to determine whether leptin affects the alloimmune response. We used an allogeneic skin transplant model as a means to analyze the allograft immune response in Lepob/ob and wild-type mice. Leptin deficiency results in an increased frequency of Treg and Th2 cells and a prolonged graft survival. These effects of leptin deficiency indicate the importance of leptin and obesity in modulating the allograft immune responses. Our data suggest a possible explanation for the increased susceptibility of hyperleptinemic obese patients to acute and chronic graft rejection. (AU)

• FAPESP's process: 07/07139-3 - The role of heme oxygenase 1 in different renal inflammatory process in experimental animal models
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• FAPESP's process: 09/50450-7 - Adipokines in experimental transplantation: interaction between leptin and the development of immunological tolerance
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• FAPESP's process: 08/58564-9 - Study of adaptive immune response modulation by the sympathetic nervous system: emphasis on autoimmunity, Th17 cells and Foxp3 + regulatory T cells
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