Cell death is a crucial event that maintains tissue homeostasis, with cell death being an important mediator of tissue repair and inflammation. Consequently, many organisms can sense both damage and pathogens by damage- and pathogen-associated molecular patterns (DAMPs and PAMPs, respectively) that are recognised by Pattern-recognition receptors (PRRs). The PRR family consists of Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), and DNA sensors such as DNA-induced activator of interferon (DAI) and cyclic GMP-AMP synthase (cGAS). Triggering of PRRs results in the induction of inflammatory cytokines and chemokines including, among others, TNF, IL-1 and type I IFNs. These cytokines play crucial roles in triggering innate immune responses by binding to their respective receptors, including TNF receptor superfamily members. Each of these pathways converge in the induction of inflammatory gene programs and cell death. There are many ways in which cells can die and this is dictated by different cell death programs which are highly interlinked. Generally, necroptosis and pyroptosis are highly immunogenic, due to the release of immunogenic factors. It has been widely believed that apoptosis is immunologically silent, however this concept has recently been challenged. Immunogenic apoptosis has been found to be induced by particular chemotherapeutics or by physical therapeutic modalities, such as ionising radiation or photodynamic therapy.
It is not only the mode of cell death itself to dictate immunogenicity, but also the inflammatory pathways that are concomitantly activated, and the consequent release of immunogenic factors. The decision between survival and death and the cell death programs that are activated will determine a pathophysiological outcome. Therefore, it is important to define which and how cell death processes shape immune responses in health and disease.
The goal of this research topic is to broaden our understanding of the factors released by dying cells and how they interact with surrounding “bystander” cells to regulate pathophysiological processes. It also aims to uncover the etiology of disease and identify means to tackle disease in a targeted manner.
This Research Topic highly welcomes original research articles, review manuscripts and methods articles covering, but not restricted to:
• The implication of various kinds of inflammatory cell death in disease
• The secretome of cells undergoing immunogenic apoptosis.
• Secretome of cells undergoing pyroptosis in response to pathogenic infection
• Secretome of cells undergoing necroptosis in response to cellular damage
• Secretome of cells undergoing ferroptosis
Keywords:
cell death, secretome, inflammation, cytokines, necroptosis, pyroptosis
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
Cell death is a crucial event that maintains tissue homeostasis, with cell death being an important mediator of tissue repair and inflammation. Consequently, many organisms can sense both damage and pathogens by damage- and pathogen-associated molecular patterns (DAMPs and PAMPs, respectively) that are recognised by Pattern-recognition receptors (PRRs). The PRR family consists of Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), and DNA sensors such as DNA-induced activator of interferon (DAI) and cyclic GMP-AMP synthase (cGAS). Triggering of PRRs results in the induction of inflammatory cytokines and chemokines including, among others, TNF, IL-1 and type I IFNs. These cytokines play crucial roles in triggering innate immune responses by binding to their respective receptors, including TNF receptor superfamily members. Each of these pathways converge in the induction of inflammatory gene programs and cell death. There are many ways in which cells can die and this is dictated by different cell death programs which are highly interlinked. Generally, necroptosis and pyroptosis are highly immunogenic, due to the release of immunogenic factors. It has been widely believed that apoptosis is immunologically silent, however this concept has recently been challenged. Immunogenic apoptosis has been found to be induced by particular chemotherapeutics or by physical therapeutic modalities, such as ionising radiation or photodynamic therapy.
It is not only the mode of cell death itself to dictate immunogenicity, but also the inflammatory pathways that are concomitantly activated, and the consequent release of immunogenic factors. The decision between survival and death and the cell death programs that are activated will determine a pathophysiological outcome. Therefore, it is important to define which and how cell death processes shape immune responses in health and disease.
The goal of this research topic is to broaden our understanding of the factors released by dying cells and how they interact with surrounding “bystander” cells to regulate pathophysiological processes. It also aims to uncover the etiology of disease and identify means to tackle disease in a targeted manner.
This Research Topic highly welcomes original research articles, review manuscripts and methods articles covering, but not restricted to:
• The implication of various kinds of inflammatory cell death in disease
• The secretome of cells undergoing immunogenic apoptosis.
• Secretome of cells undergoing pyroptosis in response to pathogenic infection
• Secretome of cells undergoing necroptosis in response to cellular damage
• Secretome of cells undergoing ferroptosis
Keywords:
cell death, secretome, inflammation, cytokines, necroptosis, pyroptosis
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.