Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL, United States.
Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL, United States.
Front Immunol. 2020 Sep 2;11:2060. doi: 10.3389/fimmu.2020.02060. eCollection 2020.
Obesity, similar to aging, is associated with chronic low-grade systemic inflammation, known as inflammaging, and represents a significantly higher risk for developing chronic diseases typical of old age. Immune cells are recruited to the obese adipose tissue (AT) by chemotactic molecules secreted by non-immune and immune cells in the AT, both contributing to the release of several pro-inflammatory mediators that fuel local and systemic inflammation, to the refractory response of immune cells to further and stimulation and to the induction of autoimmune B cells with potentially pathogenic repertoires. In terms of molecular mechanisms involved, leptin, an adipokine secreted primarily by adipocytes, has been proposed to be involved in the reduced generation of protective antibodies, and in the increased generation of autoimmune antibodies, further supporting the concept that obesity accelerates age defects. Leptin has also been shown to induce intrinsic B cell inflammation and B cell immunosenescence. The results presented in this review highlight the importance of weight reduction programs to improve immunity and reduce the risk for developing chronic diseases in obese and older individuals.
肥胖与衰老相似，与慢性低度全身炎症有关，称为炎症衰老，代表着发展为老年期典型慢性疾病的风险显著增加。趋化分子将免疫细胞募集到肥胖的脂肪组织（AT）中，这些趋化分子由 AT 中的非免疫细胞和免疫细胞分泌，两者都有助于释放几种促炎介质，这些介质引发局部和全身炎症、免疫细胞对进一步刺激的难治性反应以及潜在致病性库的自身免疫 B 细胞的诱导。就涉及的分子机制而言，瘦素是一种主要由脂肪细胞分泌的脂肪因子，据推测它参与了保护性抗体生成减少和自身抗体生成增加，进一步支持肥胖加速年龄缺陷的概念。瘦素还被证明可诱导固有 B 细胞炎症和 B 细胞免疫衰老。本综述中提出的结果强调了减肥计划的重要性，以改善肥胖和老年人的免疫力并降低患慢性疾病的风险。
