Pinheiro-Machado Erika, Gurgul-Convey Ewa, Marzec Michal T
Department of Pathology and Medical Biology, University Medical Center Groningen, Groningen, Netherlands.
Institute of Clinical Biochemistry, Hannover Medical School, Hannover, Germany.
Arch Med Sci. 2020 Jan 31;19(4):895-911. doi: 10.5114/aoms.2020.92674. eCollection 2023.
The immune system is frequently described in the context of its protective function against infections and its role in the development of autoimmunity. For more than a decade, the interactions between the immune system and metabolic processes have been reported, in effect creating a new research field, termed immunometabolism. Accumulating evidence supports the hypothesis that the development of metabolic diseases may be linked to inflammation, and reflects, in some cases, the activation of immune responses. As such, immunometabolism is defined by 1) inflammation as a driver of disease development and/or 2) metabolic processes stimulating cellular differentiation of the immune components. In this review, the main factors capable of altering the immuno-metabolic communication leading to the development and establishment of obesity and diabetes are comprehensively presented. Tissue-specific immune responses suggested to impair metabolic processes are described, with an emphasis on the adipose tissue, gut, muscle, liver, and pancreas.
免疫系统通常是在其抗感染的保护功能以及自身免疫发展中的作用背景下被描述的。十多年来,免疫系统与代谢过程之间的相互作用已有报道,实际上形成了一个新的研究领域,即免疫代谢。越来越多的证据支持这样一种假说,即代谢性疾病的发展可能与炎症有关,并且在某些情况下反映了免疫反应的激活。因此,免疫代谢的定义为:1)炎症作为疾病发展的驱动因素和/或2)刺激免疫成分细胞分化的代谢过程。在这篇综述中,全面介绍了能够改变免疫代谢通讯从而导致肥胖和糖尿病发生及发展的主要因素。描述了被认为会损害代谢过程的组织特异性免疫反应,重点是脂肪组织、肠道、肌肉、肝脏和胰腺。