Abstract
Innate and adaptive immune responses have a well-known link and represent the distinctive origins of several diseases, many of which may be the consequence of the loss of balance between these two responses. Indeed, autoinflammation and autoimmunity represent the two extremes of a continuous spectrum of pathologic conditions with numerous overlaps in different pathologies. A common characteristic of these dysregulations is represented by hyperinflammation, which is an exaggerated response of the immune system, especially involving white blood cells, macrophages, and inflammasome activation with the hyperproduction of cytokines in response to various triggering stimuli. Moreover, hyperinflammation is of great interest, as it is one of the main manifestations of COVID-19 infection, and the cytokine storm and its most important components are the targets of the pharmacological treatments used to combat COVID-19 damage. In this context, the purpose of our review is to provide a focus on the pathogenesis of autoinflammation and, in particular, of hyperinflammation in order to generate insights for the identification of new therapeutic targets and strategies.
Highlights
Accepted: 12 October 2021Autoinflammation, as an autoimmune response, is due to the excessive activation of the immune system and shows a clinical phenotype characterized by alternating periods of exacerbation and remission [1]
These diseases present a clinical picture that varies naturally according to the specific causative genetic mutations, and they are characterized by the presence of continuous or sub-continuous inflammation caused by the release of specific cytokines, with onset in the first months/years of life presenting with fever, joint involvement, skin manifestations, and serological markers [34]
It has been noted that vaccines play an important role in training innate immunity, and this evidence could partly help to understand the reason why children, subject to vaccinations in the early years of life, are the category least affected by coronavirus infection [188,189,190]
Summary
Autoinflammation, as an autoimmune response, is due to the excessive activation of the immune system and shows a clinical phenotype characterized by alternating periods of exacerbation and remission [1]. The pleiotropic role of T cell effectors (Th1 and Th17) in the mechanism of autoinflammation is evident in the pathogenesis of atherosclerosis [13]: the T-mediated immune response in atherosclerosis presents an altered balance between effector T cells and Treg cells, and the effects of these cells lead to vulnerable plaques that can break and cause thrombotic events [14,15]. Both cell types play a central role in inflammation associated with atherosclerotic lesions. The focus of this manuscript is to describe how the inflammasome platform, hyperinflammation, and cytokine secretion may be useful for identifying effective therapeutic targets for other diseases with the same involvement
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