Weight-dependent changes of immune system in adipose tissue:: Importance of leptin
Weight-dependent changes of immune system in adipose tissue:: Importance of leptin
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DOI：
10.1016/j.yexcr.2006.03.023
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发表时间：
2006-07-15
影响因子：
3.7
通讯作者：
Penicaud, L.
中科院分区：
文献类型：
--
作者：
Caspar-Bauguil, S.;Cousin, B.;Penicaud, L.
祖淋巴样细胞存在于脂肪组织中，并且它们的数量在肥胖中高度改变。瘦素的产生与脂肪质量相关，强烈参与脂肪组织和免疫系统之间的关系。我们研究了附睾（EPI）和腹股沟（ING）脂肪垫，以确定1）淋巴细胞表型是否与组织重量相关，2）瘦素是否参与这种关系。免疫组化分析显示，T和NK淋巴细胞的间质血管组分和脂肪细胞之间的紧密关系。我们确定了显着的负相关和正相关EPI重量和NK细胞和总T细胞的百分比分别通过细胞荧光分析。NK和祖先γ δ T细胞含量直接依赖于瘦素，因为它们在高脂（HF）饮食小鼠中显著增加，但与对照相比，在瘦素缺陷（ob/ob）小鼠中不显著增加。相比之下，α β T细胞含量似乎独立于瘦素，因为它们的百分比随着EPI体重的增加而显著增加，无论小鼠的类型（对照、HF、ob/ob）如何。本研究表明，脂肪组织，根据其定位，不同的免疫机制，可能参与调节脂肪细胞的功能和增殖。(c)2006年爱思唯尔公司All rights reserved.
Ancestral lymphoid cells reside in adipose tissues, and their numbers are highly altered in obesity. Leptin, production:of which is correlated to fat mass, is strongly involved in the relationships between adipose tissues and immune system. We investigated in epididymal (EPI) and inguinal (ING) fat pads to determine whether 1) lymphocyte phenotypes were correlated to the tissue weight and 2) leptin was involved in such relationships. Immunohistological analyses revealed a tight relationship between the T and NK lymphocytes of the stromal vascular fraction and adipocytes. We identified a significant negative and positive correlation between EPI weight and the percentage of NK and total T cells respectively by cytofluorometric analyses. The NK and ancestral y delta T cell contents were directly dependent of leptin since they increased significantly in high-fat (HF) diet mice but not in leptin-deficient (ob/ob) mice as compared to control. By contrast, the alpha beta T cell content seemed independent of leptin because their percentages increased significantly with the EPI weight whatever the type of mice (control, HF, ob/ob). The present study suggests that adipose tissues present, according to their localization, different immunological mechanisms that might be involved in the regulation of adipose cells functions and proliferations. (c) 2006 Elsevier Inc. All rights reserved.