作者: Elizabeth Papathanassoglou , Karim El-Haschimi , Xian Chang Li , Giuseppe Matarese , Terry Strom
DOI: 10.4049/JIMMUNOL.176.12.7745
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摘要: Leptin has direct effects not only on neuroendocrine function and metabolism, but also T cell-mediated immunity. We report in this study that leptin receptor (ObR) is expressed resting normal mouse CD4(+), CD8(+), B cells, monocyte/macrophages. ObR expression up-regulated following cell activation, with different kinetics, lymphocyte subsets. binding to results increased STAT-3 activation a pattern vs anti-CD3 Ab stimulated cells. promotes survival vitro by suppressing Fas-mediated apoptosis. lymphocytes appear be more susceptible the antiapoptotic of leptin, they show higher surface ObR, compared Moreover, CD4(+) cells isolated from ObR-deficient mice displayed reduced proliferative response, controls. Furthermore, ObR/STAT-3-mediated signaling decreased diet-induced obese model obesity resistance. In summary, our findings subsets, plays role survival, alters Taken together, data further support notion nutritional status acting via leptin-dependent mechanisms may alter nature vigor immune response.