PubMed · 5748517
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Y Yamamura, S Iijima. 1968. [Personal communication on inflammation].. https://pubmed.ncbi.nlm.nih.gov/5748517/
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Pathogens utilize many strategies to dampen the host inflammatory response. In this issue of Immunity, a report by Johnston and colleagues reveals a poxvirus strategy that inhibits the inflammasome, arresting secretion of interleukin-1-related cytokines, thus silencing key alarms that mobilize host defenses.
The PPARs transduce a wide variety of signals, including environmental and nutritional events, into a defined and ordered set of cellular responses at the transcriptional level. It has now been shown that all three PPAR isoforms (alpha, beta/delta and gamma) can participate in the regulation of inflammation responses. The ability of the PPARs to regulate inflammatory responses is a result of their transactivation and transrepression capacities. Most of the anti-inflammatory properties of the PPARs arise through their ability to antagonize nuclear factor-kappaB (NF-kappaB) and AP1 signaling pathways. By inhibiting these inflammatory transcription factors, the PPARs repress the expression of several genes that are involved in the inflammatory responses. In this review, I focus on emerging knowledge about PPARs roles in inflammatory responses.
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