Pattern recognition is an evolutionarily conserved immune process critical for multi-cellular organisms to discriminate self from non-self. Compared with terrestrial vertebrate animals, fish must cope with an even greater abundance of microorganisms from dynamically changing aquatic environments. The adaptive immune system exhibits a huge repertoire of lymphoid cell-surface receptors. However, the innate immune system employs a limited number of receptors, called pattern recognition receptors (PRRs), to recognize pathogen-associated molecular patterns (PAMPs) presented exclusively in microorganisms and damage-associated molecular patterns (DAMPs). Plasma membrane PRRs, e.g., Toll-like receptors, mainly recognize extracellular microbial reagents, activate downstream MyD88-dependent and MyD88-independent signaling pathways and increase immune gene expression in response to infection. Intracellular PRRs, including Nod-like receptors and RIG-I like receptors, are capable of sensing intracellular pathogenic molecules. The receptor-mediated canonical inflammasome and inflammatory caspase-mediated non-canonical inflammasome contribute to pro-inflammatory cytokine (e.g., interleukin-1ß) maturation and secretion, eventually leading to a pro-inflammatory immune response. Pathogens can hijack the innate immune response, leading to immunologically “silent” forms of programmed cell death, e.g., apoptosis and autophagy. This can also lead to an immunologically “violent” form of programmed cell death, e.g., pyroptosis. Pathogens can manipulate the death associated signaling pathways through different virulence factors and alter the cell death fate during infection. This altered cell death exerts a significant effect on pathogenesis.
In contrast to mammals, fish, including jawless fish, cartilaginous fish and bony fish, represent a lower form of vertebrates but are the most diverse group. This huge genomic diversity lays the molecular foundation for a novel and distinct functionally significant mechanism of immune recognition and cell death modulation. Identification of functionally significant PRRs is important for us to understand how the fish immune system distinguishes different environmental microorganisms. Moreover, the activation of downstream signaling pathways and the immune effect of programmed cell death are of great importance in revealing the molecular mechanism of pathogenesis and even therapeutic intervention in various fish diseases.
This Research Topic focuses on the immune recognition and its downstream immune response, focusing on programmed cell death in fish. We welcome Original Research, Review and Perspective articles related to, but not limited to, the following topics:
-Identification and functional studies of novel pattern recognition receptors
-New biological function of pattern recognition receptors
-Molecular basis of interaction between pattern recognition receptor and pathogen
-Identification of canonical and non-canonical inflammasome components
-Canonical and non-canonical inflammasome assembly and activation
-Inflammasome-mediated downstream inflammatory immune response
-Pathogenic virulence factor induced programmed cell death
-Molecular mechanism of programmed cell death
-The immune effect of cell death on pathogenesis
-Potential approaches to enhance anti-infection immune response
-Evolutionary and comparative aspects to immune recognition, inflammasome activation and programmed cell death
Pattern recognition is an evolutionarily conserved immune process critical for multi-cellular organisms to discriminate self from non-self. Compared with terrestrial vertebrate animals, fish must cope with an even greater abundance of microorganisms from dynamically changing aquatic environments. The adaptive immune system exhibits a huge repertoire of lymphoid cell-surface receptors. However, the innate immune system employs a limited number of receptors, called pattern recognition receptors (PRRs), to recognize pathogen-associated molecular patterns (PAMPs) presented exclusively in microorganisms and damage-associated molecular patterns (DAMPs). Plasma membrane PRRs, e.g., Toll-like receptors, mainly recognize extracellular microbial reagents, activate downstream MyD88-dependent and MyD88-independent signaling pathways and increase immune gene expression in response to infection. Intracellular PRRs, including Nod-like receptors and RIG-I like receptors, are capable of sensing intracellular pathogenic molecules. The receptor-mediated canonical inflammasome and inflammatory caspase-mediated non-canonical inflammasome contribute to pro-inflammatory cytokine (e.g., interleukin-1ß) maturation and secretion, eventually leading to a pro-inflammatory immune response. Pathogens can hijack the innate immune response, leading to immunologically “silent” forms of programmed cell death, e.g., apoptosis and autophagy. This can also lead to an immunologically “violent” form of programmed cell death, e.g., pyroptosis. Pathogens can manipulate the death associated signaling pathways through different virulence factors and alter the cell death fate during infection. This altered cell death exerts a significant effect on pathogenesis.
In contrast to mammals, fish, including jawless fish, cartilaginous fish and bony fish, represent a lower form of vertebrates but are the most diverse group. This huge genomic diversity lays the molecular foundation for a novel and distinct functionally significant mechanism of immune recognition and cell death modulation. Identification of functionally significant PRRs is important for us to understand how the fish immune system distinguishes different environmental microorganisms. Moreover, the activation of downstream signaling pathways and the immune effect of programmed cell death are of great importance in revealing the molecular mechanism of pathogenesis and even therapeutic intervention in various fish diseases.
This Research Topic focuses on the immune recognition and its downstream immune response, focusing on programmed cell death in fish. We welcome Original Research, Review and Perspective articles related to, but not limited to, the following topics:
-Identification and functional studies of novel pattern recognition receptors
-New biological function of pattern recognition receptors
-Molecular basis of interaction between pattern recognition receptor and pathogen
-Identification of canonical and non-canonical inflammasome components
-Canonical and non-canonical inflammasome assembly and activation
-Inflammasome-mediated downstream inflammatory immune response
-Pathogenic virulence factor induced programmed cell death
-Molecular mechanism of programmed cell death
-The immune effect of cell death on pathogenesis
-Potential approaches to enhance anti-infection immune response
-Evolutionary and comparative aspects to immune recognition, inflammasome activation and programmed cell death
