Trained Immunity and Endotoxin Tolerance in Inflammatory Diseases

Dear Colleagues,

Innate immune cells have been shown to be able to articulate non-specific memory-like responses known as trained immunity (or innate memory; abb. TRIM), manifested with increased responsiveness against secondary pathogenic insults. Contrary to trained immunity, endotoxin tolerance is a well-known immune reaction characterized by declined responsiveness and increased repairing/anti-inflammatory reactions. Both of these opposing adaptive features of the innate immune system are shaped by different external and internal stressors, promoted mainly by epigenetic changes (including histone methylation or acetylation) with resulting changes in metabolism (glycolysis, glutaminolysis, the accumulation of fumarate, fatty acid oxidation, or itaconate pathway) and mediated particularly by the phosphoinositide 3-kinase (PI3K)/mechanistic target of the rapamycin (mTOR) pathway. Recent advances have revealed that trained memory as well as tolerance may alter several cellular functions such as migration, phagocytosis, killing abilities, and anti-microbial properties. This then has a major impact on the progression or suppression of different inflammatory diseases (i.e., allergies, atherosclerosis, asthma, obesity, sepsis, autoimmune diseases, transplant rejection, multi-system inflammatory syndrome (COVID-19)). The inappropriate induction of one of these antagonistic adaptive manners may result in maladaptive reactions which trigger life-threating events. As such, we invite all the colleagues to submit their findings in this Special Issue to further provide more insights on the role of the trained immunity and tolerance development in inflammatory disorders.  

Dr. Trim Lajqi
Dr. Christian Gille
Dr. Hannes Hudalla
Guest Editors

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• innate memory
• tolerance
• signaling
• metabolism
• epigenetics
• inflammatory diseases