While inflammatory responses are essential for survival to pathogen exposure, unresolved inflammation fosters and supports a wide range of human pathologies, including autoimmune, infectious and malignant diseases. Such dysregulation of inflammation plays a prominent role in virus-induced pathologies as highlighted by cytokine storms, which are frequently associated with viral infections and account for a large number of virus-associated deaths. Similarly, chronic cancer-associated inflammation also feeds many cancer-associated comorbidities that ultimately cause patients demise. While the genetic or etiologic causes for these pathologies are extremely diverse, the molecular processes leading to the onset and maintenance of chronic, unresolved cytokine release are likely to have a common ground.
The field of innate immunity has seen profound conceptual changes in recent years, with the quick rise of the nucleic acid immunity field, based on the emerging notion that self-nucleic acids constitute potent inducers of chronic inflammation. Immune-stimulatory nucleic acids constitute pathogen-associated molecular patterns (PAMPs) similar to those coming from bacteria and viruses. Over the past years, several pathogen recognition receptors and downstream signalling have been identified, that promote the production of pro-inflammatory mediators. These receptors have also been demonstrated to play a role in the immunity induced by self-nucleic acids, known as damage-associated molecular patterns (DAMPs). While a tremendous amount of studies have aimed to decipher the pathways involved in the onset of cytokine production in response to immune-stimulatory nucleic acids, there are still several unanswered major questions.
In particular, the crosstalk and orchestration of these coexisting pathways should be evaluated in the presence of various nucleic acid substrates. An additional level of complexity arises from the notion that innate immune responses, rather than being ubiquitous, harbor cell type- or tissues-specificity. Comparative analyses of innate immune responses in different species will be instrumental to identify the universal and species-specific components of these responses and evaluate their evolution under distinct selective pressures such as pathogen infections. Understanding these processes will be crucial to better understand the basics of the inflammatory response, and, in turn, open the way for the identification of personalized treatments against inflammatory diseases of various origins.
This Research topic aims to group Reviews, Systematic Reviews, Mini reviews, Hypothesis and Theory, Perspective, or Opinion articles, in order to draw a comprehensive overview of the current knowledge in nucleic acid immunity and to address how this may contribute to a better understanding of deleterious inflammation, including cytokine storms, for the design of therapeutic approaches. We welcome manuscripts covering, but not limited to, the following topics:
• Nucleic acid immunity
• Nucleic acid receptors and downstream signalling pathways
• Pathogen-induced inflammation
• Self nucleic acids- and cytokine storms- associated inflammation and cancer
• Innovations on models and technology for the study of nucleic acid associated inflammatory diseases (zebrafish, murine, other)
While inflammatory responses are essential for survival to pathogen exposure, unresolved inflammation fosters and supports a wide range of human pathologies, including autoimmune, infectious and malignant diseases. Such dysregulation of inflammation plays a prominent role in virus-induced pathologies as highlighted by cytokine storms, which are frequently associated with viral infections and account for a large number of virus-associated deaths. Similarly, chronic cancer-associated inflammation also feeds many cancer-associated comorbidities that ultimately cause patients demise. While the genetic or etiologic causes for these pathologies are extremely diverse, the molecular processes leading to the onset and maintenance of chronic, unresolved cytokine release are likely to have a common ground.
The field of innate immunity has seen profound conceptual changes in recent years, with the quick rise of the nucleic acid immunity field, based on the emerging notion that self-nucleic acids constitute potent inducers of chronic inflammation. Immune-stimulatory nucleic acids constitute pathogen-associated molecular patterns (PAMPs) similar to those coming from bacteria and viruses. Over the past years, several pathogen recognition receptors and downstream signalling have been identified, that promote the production of pro-inflammatory mediators. These receptors have also been demonstrated to play a role in the immunity induced by self-nucleic acids, known as damage-associated molecular patterns (DAMPs). While a tremendous amount of studies have aimed to decipher the pathways involved in the onset of cytokine production in response to immune-stimulatory nucleic acids, there are still several unanswered major questions.
In particular, the crosstalk and orchestration of these coexisting pathways should be evaluated in the presence of various nucleic acid substrates. An additional level of complexity arises from the notion that innate immune responses, rather than being ubiquitous, harbor cell type- or tissues-specificity. Comparative analyses of innate immune responses in different species will be instrumental to identify the universal and species-specific components of these responses and evaluate their evolution under distinct selective pressures such as pathogen infections. Understanding these processes will be crucial to better understand the basics of the inflammatory response, and, in turn, open the way for the identification of personalized treatments against inflammatory diseases of various origins.
This Research topic aims to group Reviews, Systematic Reviews, Mini reviews, Hypothesis and Theory, Perspective, or Opinion articles, in order to draw a comprehensive overview of the current knowledge in nucleic acid immunity and to address how this may contribute to a better understanding of deleterious inflammation, including cytokine storms, for the design of therapeutic approaches. We welcome manuscripts covering, but not limited to, the following topics:
• Nucleic acid immunity
• Nucleic acid receptors and downstream signalling pathways
• Pathogen-induced inflammation
• Self nucleic acids- and cytokine storms- associated inflammation and cancer
• Innovations on models and technology for the study of nucleic acid associated inflammatory diseases (zebrafish, murine, other)
