Abstract
Pattern Recognition Receptors (PRRs) are proteins capable of recognizing molecules frequently found in pathogens (the so-called Pathogen-Associated Molecular Patterns—PAMPs), or molecules released by damaged cells (the Damage-Associated Molecular Patterns—DAMPs). They emerged phylogenetically prior to the appearance of the adaptive immunity and, therefore, are considered part of the innate immune system. Signals derived from the engagement of PRRs on the immune cells activate microbicidal and pro-inflammatory responses required to eliminate or, at least, to contain infectious agents. Molecularly controlled forms of cell death are also part of a very ancestral mechanism involved in key aspects of the physiology of multicellular organism, including the elimination of unwanted, damaged or infected cells. Interestingly, each form of cell death has its particular effect on inflammation and on the development of innate and adaptive immune responses. In this review article, we discuss some aspects of the molecular interplay between the cell death machinery and signals initiated by the activation of PRRs by PAMPs and DAMPs.
Highlights
In 1989, Charles Janeway Jr. proposed the existence of a collection of receptors expressed by innate immune cells responsible for detecting conserved products of microbial origin [1]
Macrophages and dendritic cells (DCs) reside on the center of these two arms of immunity
Through the interaction with conserved molecular patterns frequently associated with pathogens (PAMPs), Pattern Recognition Receptors (PRRs) trigger a series of biochemical signaling cascades that activates proinflammatory programs on DCs that enable the differentiation of antigen-specific T cells into protective effector TH1, TH2, and TH17 cells
Summary
In 1989, Charles Janeway Jr. proposed the existence of a collection of receptors expressed by innate immune cells responsible for detecting conserved products of microbial origin [1]. Despite the different mechanisms that initiate necroptosis, in all cases cells undergo rapid MLKL-mediated plasma membrane permeabilization with consequent release of intracellular contents, including many DAMPs, such as lysosomal proteases, DNA, mtDNA, ATP, and HMGB1 [(55); Table 1].
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