| Content Provider |
World Health Organization (WHO)-Global Index Medicus |
| Author |
Rogoz, Aneta Cohn, Lillian B. Lee, Kihyun Fanok, Melania H. Domingos, Ana I. Amoury, Manal Mucida, Daniel Reis, Bernardo S. Dallner, Olof S. Mascaraque, Cristina Moraes-Vieira, Pedro M. |
| Description |
Author Affiliation: Reis BS ( Laboratory of Mucosal Immunology, The Rockefeller University, New York, NY 10065); Lee K ( Laboratory of Mucosal Immunology, The Rockefeller University, New York, NY 10065); Fanok MH ( Laboratory of Mucosal Immunology, The Rockefeller University, New York, NY 10065); Mascaraque C ( Laboratory of Mucosal Immunology, The Rockefeller University, New York, NY 10065); Amoury M ( Laboratory of Mucosal Immunology, The Rockefeller University, New York, NY 10065); Cohn LB ( Laboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065); Rogoz A ( Laboratory of Mucosal Immunology, The Rockefeller University, New York, NY 10065); Dallner OS ( Laboratory of Molecular Genetics, The Rockefeller University, New York, NY 10065); Moraes-Vieira PM ( Division of Endocrinology, Diabetes and Metabolism, Beth Israel Medical Deaconess Center, Harvard Medical School, Boston, MA 02215); Domingos AI ( Obesity Laboratory, The Gulbenkian Science Institute, 2780-156 Oeiras, Portugal.); Mucida D ( Laboratory of Mucosal Immunology, The Rockefeller University, New York, NY 10065) |
| Abstract |
The hormone leptin plays a key role in energy homeostasis, and the absence of either leptin or its receptor (LepR) leads to severe obesity and metabolic disorders. To avoid indirect effects and to address the cell-intrinsic role of leptin signaling in the immune system, we conditionally targeted LepR in T cells. In contrast with pleiotropic immune disorders reported in obese mice with leptin or LepR deficiency, we found that LepR deficiency in CD4(+) T cells resulted in a selective defect in both autoimmune and protective Th17 responses. Reduced capacity for differentiation toward a Th17 phenotype by lepr-deficient T cells was attributed to reduced activation of the STAT3 and its downstream targets. This study establishes cell-intrinsic roles for LepR signaling in the immune system and suggests that leptin signaling during T cell differentiation plays a crucial role in T cell peripheral effector function. |
| ISSN |
00221767 |
| e-ISSN |
15506606 |
| DOI |
10.4049/jimmunol.1402996 |
| Journal |
The Journal of Immunology |
| Issue Number |
11 |
| Volume Number |
194 |
| Language |
English |
| Publisher |
The American Association of Immunologists |
| Publisher Date |
2015-06-01 |
| Publisher Place |
United States |
| Access Restriction |
Open |
| Subject Keyword |
Cell Differentiation Immunology Leptin Obesity Receptors, Leptin Th17 Cells Cytology Animals Autoimmunity Genetics Cells, Cultured Citrobacter Rodentium Colitis Enterobacteriaceae Infections Lymphocyte Activation Mice Mice, Inbred C57bl Mice, Knockout Stat3 Transcription Factor Signal Transduction Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology |
| Content Type |
Text |
| Resource Type |
Article |
| Subject |
Immunology and Allergy Immunology |
