Please use this identifier to cite or link to this item:
https://hdl.handle.net/20.500.14279/1903
Title: | Leptin receptor expression and signaling in lymphocytes: kinetics during lymphocyte activation, role in lymphocyte survival, and response to high fat diet in mice |
Authors: | Papathanassoglou, Elizabeth El-Haschimi, Karim Li, Xian Chang |
Major Field of Science: | Medical and Health Sciences |
Field Category: | Basic Medicine |
Keywords: | Immunology;Lymphocytes;Mice;Antigens;Cells |
Issue Date: | 15-Jun-2006 |
Source: | The Journal of Immunology, 2006, vol. 176, no.12, pp. 7745-7752 |
Volume: | 176 |
Issue: | 12 |
Start page: | 7745 |
End page: | 7752 |
Journal: | The Journal of Immunology |
Abstract: | Leptin has direct effects not only on neuroendocrine function and metabolism, but also on T cell-mediated immunity. We report in this study that leptin receptor (ObR) is expressed on resting normal mouse CD4 +, CD8 +, B cells, and monocyte/macrophages. ObR expression is up-regulated following cell activation, but with different kinetics, in different lymphocyte subsets. Leptin binding to ObR results in increased STAT-3 activation in T cells, with a different activation pattern in resting vs anti-CD3 Ab stimulated T cells. Leptin also promotes lymphocyte survival in vitro by suppressing Fas-mediated apoptosis. B lymphocytes appear to be more susceptible to the antiapoptotic effects of leptin, and they show higher surface expression of ObR, compared with T cells. Moreover, CD4 + T cells isolated from ObR-deficient mice displayed a reduced proliferative response, compared with normal controls. Furthermore, ObR/STAT-3-mediated signaling in T lymphocytes is decreased in the diet-induced obese mouse model of obesity and leptin resistance. In summary, our findings show that the ObR is expressed on normal mouse lymphocyte subsets, that leptin plays a role in lymphocyte survival, and that leptin alters the ObR/STAT-3-mediated signaling in T cells. Taken together, our data further support the notion that nutritional status acting via leptin-dependent mechanisms may alter the nature and vigor of the immune response. Copyright |
URI: | https://hdl.handle.net/20.500.14279/1903 |
ISSN: | 15506606 |
DOI: | 10.4049/jimmunol.176.12.7745 |
Rights: | © The American Association of Immunologists |
Type: | Article |
Affiliation: | Beth Israel Deaconess Medical Center |
Affiliation : | Harvard University |
Publication Type: | Peer Reviewed |
Appears in Collections: | Άρθρα/Articles |
CORE Recommender
This item is licensed under a Creative Commons License